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COPVRIGHT DEPOSIT. 



MASTITIS OF THE COW 



BY 

SVEN WALL 

ASSISTANT IN THE VETERINARY HIGH SCHOOL AT STOCKHOLM 



WITH 29 ILLUSTRATIONS 



AUTHORIZED TRANSLATION WITH ANNOTATIONS 
BY 

DR. WALTER J. CROCKER. B.S., V.M.D. 

PBOFEBSOB OF VETERINABT PATHOLOOY, UNIVERSITY OF PENNSYLVANIA 




PHILADELPHIA AND LONDON 
J. B. LIPPINCOTT COMPANY 






COPTRIGHT, I918, BT J. B. I.IPPINCOTT COMPANT 



Electrolyped and Printed by J. B. Lippincott Company 
The Washington Square Press, Philadelphia, V. 6. A. 



MAY 22 1918 

©CLA4y7428 



TRANSLATOR'S PREFACE 

The dearth of detailed scientific and practical literature 
on the subject of inflammation of the udder in cows 
prompted me to prepare a translation of Professor Sven 
Wall's excellent book, " Die Euterentzundungen der Kuh.'* 

Not only is the subject adequately treated in all its im- 
portant practical relationships, but the conclusions drawn 
have been established upon sound principles of pathology 
and by decisive animal experimentation. The tubulo-alveo- 
lar system, Professor Wall observes, is lined by epithelium, 
cubical and flat, which constitutes the parenchymatous tis- 
sue. This is supported by interstitial connective tissue 
which constitutes the stroma. 

Bacterial invasion of the interstitial connective tissue 
comprises a stroma-infection, the presence of which is mani- 
fested, more or less obviously, by a reaction on the part of 
the body to the bacterial irritation called an inflammation 
or interstitial mastitis. This may be primary or secondary 
depending upon the manner of its inception, or acute or 
chronic depending upon its duration and the character of 
the specific etiological factors. 

Bacterial invasion of the tubulo-alveolar system or 
parenchymatous passages, and thus necessarily the milk 
which is contained in them, he calls a parenchyma-infection 
or milk-infection, the presence of which is manifested by a 
reaction on the part of the body to the bacterial irritation 
called an inflammation or parenchymatous mastitis. This 
may be primary or secondary depending upon the manner 
of inception, or acute or chronic depending upon its dura- 
tion, — and based upon the character of its inflammatory 
exudate it is classified as catarrhal mastitis, sero-hemor- 



iv TRANSLATOR'S PREFACE 

rhagic mastitis, croupous mastitis, purulent mastitis, or 
croupo-purulent mastitis. These terms indicate the pres- 
ence of an inflammatory process of the udder in which the 
parenchyma is affected with various degrees of severiti/, 
which are distinguished hy the character of their exudates. 

In the acute form of these types of parenchymatous 
mastitis, except the catarrhal type, the udder becomes 
swollen, hot, painful and more or less hard and there is a 
rather rapid diminution in the milk secretion. In catarrhal 
mastitis the milk becomes more or less altered and not much 
decreased, but the udder manifests few, if any, changes. 

Because of these clinical differences the clinician, for 
convenience, recognizes catarrhal mastitis separately as 
the same process just indicated by that name, but under 
the collective head of parenchymatous mastitis he includes 
sero-hemorrhagic, croupous, purulent and croupo-purulent 
mastitis which show hot, painful swellings and rapid dimi- 
nution in milk secretion. In addition he recognizes inter- 
stitial mastitis and gangi'enous mastitis, which complete his 
classification, i.e., catarrhal mastitis, parenchymatous mas- 
titis, interstitial mastitis, and gangrenous mastitis. 

By use of the terms udder-infection, stroma-infection, 
and milk-infection (parenchyma-infection) in lieu of mas- 
titis, interstitial mastitis, and parenchymatous mastitis re- 
spectively, terms with which we are more familiar in this 
country, the author keeps uppermost in the student's mind 
the fact that the actual presence of the bacteria in the vari- 
ous parts of the udder, and the primary lesions produced by 
their harmful influence, are the fundamental factors to be 
overcome. Not only are they to be overcome by the scien- 
tific application of prophylactic, medicinal and surgical 
remedies by the veterinarian, but mastered by elimination 
of the causative agents, the bacteria, and repair of the pri- 
mary lesions induced by them, through the agency of that 
complex reparative process of the body called an inflamma- 



TRANSLATOR'S PREFACE v 

tion, which is a reaction of the body to the action of an irri- 
tant, or an attempt on the part of the body to repair an 
injury. 

Thus the inflammation or mastitis, by the various factors 
pertaining to it, i.e., (1) alteration of tissue (primary 
lesion, degeneration, desquamation, necrosis ) , ( 2 ) emigra- 
tion of leucocytes (fluid and cellular exudates, phagocy- 
tosis), or (3) proliferation of connective tissue (repair by 
healing, false regeneration), is but the expression of the 
presence of the fundamentally interesting udder-wound, or 
udder-infection, he it stroma-infection or milk-infection. 

The foregoing co-ordination of terms used by Professor 
Wall with those most familiar to our literature precludes 
the possibility of failure on the part of the early student 
of pathology to grasp the complete significance and full 
appreciation of Professor Wall's treatise on the udder- 
inflammations of the cow. 

By the use of [ ] I have endeavored to include such 
available data as tend toward a closer application to con- 
ditions prevailing in this country, and at this time. 

Walter J. Crocker. 

Philadelphia, Pa., 
January, 1918. 



PREFACE 

This work is based upon the investigation of milk of 
diseased udders and the subsequent autopsy of such dis- 
eased udders. 

The material for these examinations consisted princi- 
pally of samples of milk and specimens of udders sent to 
the High School for the investigation of tuberculosis. 

In addition to this material, milk samples were obtained 
from acute udder-afFections which were not tuberculous. 
Most of the material examined, however, was of a tuber- 
culous character. The number of non-tuberculous udders 
amounted to ca. 50. 

In order to study the kinds of udder-infections to be 
taken up not less than seventy bacterial isolations were 
made from milk and udders by the plate method. The cul- 
ture medium was sermn-gelatin-agar or serum-agar. Gela- 
tin plates were poured in only a couple of cases and then 
for a special purpose. 

For study of the histological changes in the diseased 
udders thirty diiFerent preparations were examined. Most 
of them were cut with the freezing microtome immediately 
after fixation in formalin. The remainder, ca. 10 cases, 
were cut after imbedding in paraffin. The sections were 
stained with hasmatoxylin and eosin or after the method of 
Van Gieson. In order to study the bacteria the sections 
were stained with carbolmethylene blue or after the method 
of Weigert or Ziehl. 

Concerning the clinical description I am supported by 
clinical material from my veterinary practice (35 cases), 
and upon the cows with udder tuberculosis, purchased by 
the Veterinary High School, in which I produced mastitis 
by artificial infection. In addition other veterinarians have 



viii PREFACE 

contributed data on the clinical symptoms of the question- 
able or uncommon forms of mastitis. 

To all colleagues who have assisted me in my work 
through material submitted or written information I ex- 
tend my heartiest thanks. Finally I wish to express my 
deepest gratitude to my highly esteemed teacher, Professor 
J. Svensson, who has placed cows at my disposal and guided 
me in the technic of the bacteriological and pathologic- 
histological investigations. 

SVEN WaLI^ 
Stockholm. 



CONTENTS 



CHAPTER PAGE 

I. The Udder of the Cow 1 

Anatomical and Physiological Review. 

II. Mastitis in General 6 

III. Mastitis Caused by External Force 8 

Injuries of the Udder — Wounds of the Udder. 

IV. Infectious Mastitis in General 12 

Ports of Infection — The Teat Canal as a Port of Infection — Udder 
Wounds as Ports of Entrance — The Blood as a Port of Infection — 
Infection of the Udder in General — Milk-infection — Stroma-infection. 

V. Types of Infection 36 

VI. Udder-streptomycosis 38 

Udder-infection — Milk-infection — Atypical Chronic Streptomy- 
cosis — Stroma-infection. 

VII. Udder-staphylomycosis 54 

The Infectious Organism — Udder-infection — Milk-infection — Stroma- 
infection. 

VIII. Udder-colibacillosis 62 

Infectious Organism — Udder-infection — Milk-infection — Stroma- 
infection. 

IX. Udder-ptobacillosis 71 

Infectious Organism — Udder-infection — Stroma-infection. 

X. Udder-tuberculosis 87 

Infectious Organism — Udder-infection — Stroma-infection. 

XI. Udder-actinomycosis 106 

Infectious Organism — Udder-infection — Stroma-infection — Types. 

XII. Udder-necrobacillosis 117 

Udder-infection. 

XIII. Clinical Diagnosis of Mastitis 119 

Mastitis Caused by External Force — Udder-infection — Infected 
Udder-wounds — Genuine Udder-infections. 

ix 



X CONTENTS 

XIV. Autopsy 127 

Post-mortem Technic — Post-mortem Diagnosis — Udder-wounds — 
Solidification of the Udder. 

XV. Importance of Mastitis to Milk Control 138 

XVI. The Importance of Mastitis to Meat Inspection 144 

Examination — Judgment. 

XVII. Post-mortem Report 148 

I. Single Infections — II. Mixed Infections. 

XVIII. A Few Reports of Contagious Udder-infections 161 

I. Contagious Udder-streptomycosis — II. Contagious Udder-pyo- 
bacillosis. 



ILLUSTRATIONS 



FIG. PAGE 

1. Cross Section of Three Tubuli 2 

2- Vessels of the Udder 3 

3. Milk-infection. Staphyxx)mycosis 20 

4. Milk-infection. Colibacillosis 21 

5. Stroma-infection of Chronic Character 30 

6. The Pathogenic Streptococci in Milk Sediment 40 

7. Colonies of Streptococci 41 

8. Culture of Streptococci 41 

9. Typical Chronic Streptomycosis 40 

10. Pathogenic Staphylococci in Croupous Membrane from Udder 55 

11. Colonies of Staphylococci 55 

12. Culture of Staphylococci. Stab in Serum-gelatix-agar 56 

13. Culture of Staphylococci. Stab in Gelatin 56 

14. Colon Bacilli in Milk Sediment 63 

15. Deep Colonies of Colon Bacilli with and Without Daughter Colonies 64 

16. Surface Colony of Colon Bacilli 64 

17. Cultures of Colon Bacilli. Stab in Serum-gelatin-agar 65 

18. Culture of Colon Bacilli. Stab in Gelatin 65 

19. Pyogenes Bacilli in Milk Sediment 72 

20. Deep Colonies of Pyogenes Bacilli 73 

21. Stab Culture of Pyogenes Bacilli 73 

22. Stab Culture of Pyogenes Bacilli in Gelatin 73 

23. Tuberculosis of the Udder 90 

24. Tubercle Bacilli in Milk Sediment 102 

25. Actinomyces Colonies in Pus (X 30) 107 

26. Actinomyces Coix)xies in Pus (X 250) 107 

27. Actinomyces Colony. Cut Section (X 300) 107 

28. Actinomycosis of Udder 110 

29. Position of IL^lves of the Udder at Autopsy 127 



MASTITIS OF THE COW 

CHAPTER I 

THE UDDER OF THE COW 

Anatomical and Physiological Review 

Anatomy. — The udder is a tubulo-alveolar gland. 
Like other glands, it consists of a true secreting part, the 
parenchjnma, and a connective-tissue framework, called 
the stroma. 

The parenchyma consists of extensively branched canals 
or passages as fine as a hair, called tubuli. At their ulti- 
mate extremities or blind end they show vesicular dilata- 
tions (tubulo-alveolar gland type) which gradually con- 
verge into larger collecting ducts that finally terminate in 
cavities in the teats as large as a hen's egg, called milk cis- 
,terns. The milk cisterns empty from the ends of the teats 
through a canal the size of a match, called the teat canal. 

The walls of the finest tubules consist of a single layer 
of cubical epithelial cells. The collecting tubules, cisterns 
and teat canals are lined with several layers of epithelium. 

The parenchyma is divided by the stroma into round 
lobules as large as a pea, within which the above mentioned 
different tubules are imbedded in a very thin, fine connec- 
tive-tissue network called the intralobular connective tissue 
(Fig. 1). The part of the stroma which separates the 
single lobules is called the interlobular connective tissue. 
From this as a framework the fine intralobular connective 
tissue is given off. Blood-vessels and nerves lie in the 
stroma. 



2 MASTITIS OF THE COW 

The intralobular connective tissue is made up of fine 
fibrillary connective-tissue tufts containing large lynipli 
spaces. The interlobular connective tissue on the other 
hand is made up of firmer fibrilla showing only a few small 
spaces. 

The collecting tubes are surrounded and joined by con- 
nective tissue which becomes increasingly firmer and thicker 
and which constitutes an effectual firm connective-tissue 
membrane around the epithelium of the cisterns and the 
teat canals. 

The gross anatomical structure of the udder of the 
cow consists of four parts, the two lateral halves which 

are separated from each other by loose 
connective tissue, a left and a right 
half. These halves are again divided 
into two parts, an anterior and a pos- 
terior quarter. These are very firmly 
bound together by connective tissue. 
The udder receives blood through 
Fio. 1— Cross section of three tlic cxtcmal pudic artcry which is a 

branch of the crural artery. These ex- 
ternal pudic arteries divide into two branches, one for 
the anterior and one for the posterior quarters. The blood 
is returned through two blood-vessels: (1) the milk vein 
or subcutaneous abdominal vein, which runs anteriorly to 
the internal thoracic vein, and ( 2 ) the external pudic vein, 
which passes posteriorly (Fig. 2). 

The lymph-vessels of the udder are numerous and pass 
posteriorly to the supramammary lymph-glands and from 
here out through the internal lumbar-glands to the thoracic 
duct. 

Physiology. — The udder secretes the milk. It func- 
tionates periodically and the period depends upon preg- 
nancy; thus milk secretion begins with great quantities with 
parturition and continues for ca. 7-8 months. After this 





THE UDDER OF THE COW 3 

time the milk decreases, the cow loses tone and finally with 
difficulty gives a negligible quantity of milk which is gray- 
ish-yellow, thin and watery. 

In general the first milk secretion is produced through 
reflex stimulations at parturition. The normal milk secre- 
tion is only produced through birth. 

Milk secretion can be produced however under other 
circumstances, as during oestrum. This is of little im- 
portance, as a rule, and the udder soon loses its tone 
again (spontaneous milk secretion). 

Experimentally it is possible to 
produce an atypical milk secretion 
through stimulation of the correspond- 
ing nerves. 

The above mentioned method of 
producing milk secretion is maintained j,,^ 2._vesseis of the ud- 
through mechanical stimulation by v.«.a^'=lnTerk.repia8tric 
the sucking of the calf or by the hand v.r"'^ vena uben. 
of the milker. Without these mechani- "." =sup7amamm8ry 
cal factors the milk quickly diminishes. 

The milk secretion is therefore introduced by par- 
turition and maintained through mechanical stimulation 
(milking). 

This mechanical stimulation however cannot sustain 
the milk secretion indefinitely, as the milk secretion di- 
minishes usually about two months before the next birth. 

The lactation period can only be extended by mechani- 
cal stimulation when no impregnation has taken place. 
This can be induced for from fifteen to eighteen months, 
especially after castration; in every case however a gradual 
diminution occurs. 

In this condition the blood supply is decreased and the 
udder is poor in liquid and dry (diminished lymph). 

The reflexly produced activity of the udder cells dis- 
appears simultaneously with the blood supply and in con- 



4 MASTITIS OF THE COW 

sequence of this lessened nervous stimulation of the gland 
cells and decreased nutrition a condition of diminished 
milk secretion results. 

The quantity of milk is greatest during the first month 
after parturition but gradually decreases afterward. The 
udder decreases in circumference as it is no longer distended 
with milk and becomes small and quiescent or in the dry or 
alactiferous state. 

In consequence of the diminished work and nutrition the 
organ undergoes a process called atrophy in pathology but 
which is physiological in this case. The cell elements be- 
come smaller and their number decreases, since part of the 
cells become retrogressively altered, fatty degenerated and 
desquamated. The tubules and consequently the lobules 
become smaller in this way. At the same time, as an indi- 
cation of retrogressive alterations, great numbers of leuco- 
cytes emigrate to the intralobular connective tissue where 
they assist in the work of absorption. 

The atrophic gland cells give off other products of 
secretion. This secretion is no longer normal milk, it is 
grayish-yellow and thin, not infrequently viscid and con- 
tains a large quantity of albumin so that it coagulates on 
boiling. INIoreover it is rich in cells, epithelial cells and 
especially in emigrating leucocytes which are often laden 
with fat droplets. The secretion is resorbed for the most 
part, in which work the leucocytes are directly responsible 
as they re-enter the blood-vessels laden with fat droplets. 
The atrophic gland cells are capable of producing a yellow 
coloring matter within their structures which lends a dis- 
tinct dark yellow color to the cut surface of the yellow 
udder (yellow atrophy). 

At the next parturition the condition is immediately 
changed. The cells become stimulated to secretion and the 
atrophic udder is again well nourished with blood, conse- 
quently the cells very quickly become functionable again 
and the milk, especiallj-, very soon becomes normal. The 



THE UDDER OF THE COW 5 

atrophic pigmentation and likewise the leucoeytic infiltra- 
tion disappear. 

The milk of the first few days, the so-called colostrum, 
has an albumin and leucoeytic content of great similarity 
to the milk of the atrophic udders, the " gelt " milk. 

During this quick change from the dry to the lactation 
state circulatory disturbances may easily occur. The func- 
tional hypersemia can frequently be so increased that an 
abnormal transudation occurs inducing oedema of the udder. 
Following this condition small capillary hemorrhages may 
occur in the intralobular connective-tissue spaces from 
which blood may empty into the milk-ducts, mix with the 
milk and cause bloody milk. 

Following these changes functional disturbances may 
also develop. It is very probable that the atrophic cells 
also secrete other abnormal products, such as virulent 
toxins although in insignificant quantities. Following par- 
turition however large quantities of the same toxin may 
be produced due to the altered condition which may lead 
to a general intoxication, milk fever. This disease is treated 
by air inflation with localized cell paralysis due to the 
effect of pressure. 

Summary 

I. Anatomy of the udder : 

A. Microscopic structure. 

1. The parenchyma of the udder. 

2. The stroma of the udder. 

B. Gross anatomical structure. 

Arteries and veins. 
Lymph-vessels. 
n. Physiology of the udder: 

A. Milking period. 

B. Incitation and maintenance of milk secretion. 

C. Diminution, dry or alactiferous udder, " gelt " milk. 

D. The udder at the time of parturition. 

Circulatory disturbances. 
Functional disturbances. 



CHAPTER II 
MASTITIS IN GENERAL 

Definition. — Inflammation of the udder or mastitis 
is a local disease of the udder of a reactive character which 
manifests itself by an active hypersemia, emigration of cells, 
and proliferation of connective tissue. 

Etiology. — Mastitis is brought about through harmful 
local influences. These harmful influences are of two kinds : 
(1) physical, mechanical nature; external force; (2) chem- 
ical nature, bacterial toxin ; infection. 

Pathogenesis. — The part of the udder exposed to these 
harmful factors can consequently undergo retrogressive 
alterations and indeed become so injured that a more or 
less progressive death of cells super\^enes as the primary 
lesion.^ The ad j acent living tissue subsequently reacts with 
an inflammation. In this condition the emigi-ating cells, 
especially the leucocytes and connective-tissue cells, rid the 
local diseased area of dead cells and foreign bodies that 
might be present. The connective-tissue proliferation which 
occurs at this time is a reparative process and gradually fills 
all defects existing in the tissue by the process of healing. 

This process is supported by a rich blood supply to 
the diseased part called hyperemia, following which the 
physiological transudation is increased, and this increased 
transudate, together with emigrated cells, possibly present 
foreign bodies and dead cells, is called an exudate. 

The real position of the inflammation is in the stroma. 
The parenchyma is secondarily affected in mastitis follow- 
ing alterations in the stroma. 

In consequence of the difference in the structures of the 

^ Like Ribbert, I do not classify the retrogressive process with 
inflammation, but I maintain that it is the incentive factor of the 
inflammation, wliich therefore may best be called the primary lesion. 
[Alteration.] 
6 



MASTITIS IN GENERAL 7 

stroma, the intralobular connective tissue is the most se- 
verely affected, as it is the most loosely constructed and 
richest in juices. These spaces become filled with exudate 
which consists principally of leucocytes and connective-tis- 
sue cells. In this condition the tubules become pressed 
together and the epithelial cells undergo desquamation. 
Part of the exudate is forced into the tubules and mixed 
with the milk, which consequently becomes altered in its 
composition, especially in its cell content. At the same 
time a proliferation of the connective tissue takes place with 
thickening of the intralobular connective tissue. Similar 
alterations but of a lower grade take place in the remaining 
stroma of the inflamed part. 

During the lactation period the udder is most rich in 
juice and most sensitive, and the inflammations are there- 
fore more severe and often malignant. The dry or alac- 
tiferous udder, which is comparatively poor in fluid, is 
however less sensitive toward the external influences, and 
its inflammations are therefore milder and more benign. 

Termination. — When the irritating matter has been 
removed by the leucocytes, inflammation recedes. The exu- 
date is resorbed, leucocytes re-enter the blood- and lymph- 
vessels, and cell infiltration disappears or is reduced to a 
minimum. The intralobular connective tissue becomes 
thinner and the tubules are again dilated and enlarged. 

The original circumference of the tubules is not attained 
however, as the intralobular tissue has become thickened by 
proliferation of the connective tissue, which does not com- 
pletely reduce following a severe inflammation. As a re- 
sult of inflammation there is usually a connective tissue 
proliferation of varying degree which may terminate as 
sclerosis with subsequent diminution of tubular circumfer- 
ence or atrophy. 

Classification. — The causes of mastitis maj^ be di- 
vided into: (1) mastitis caused by external force; (2) 
mastitis caused by infection, infectious mastitis. 



CHAPTER III 

MASTITIS CAUSED BY EXTERNAL FORCE 
This mastitis may be divided into injuries and wounds. 

INJURIES OF THE UDDER 

An injury of the udder is a destruction of the udder 
tissues through a more or less uninjured skin covering. 

Causes. — Injuries of the udder may be produced by a 
blow, by squeezing or by being trod upon. 

One must discriminate between the primary effect, 
that is the primarj^ lesion produced by the direct effect of 
the external force, and the subsequent inflammation. 

Primary Lesion. — The force can produce an imme- 
diate necrosis of the softer cells, especially the epithelial 
cells, in a circumscribed area and rupture of blood- and 
lymph-vessels with an extravasation of blood and lymph 
into the intralobular connective tissue particularly. This 
hemorrhage can also get into the milk passages and give 
rise to bloody milk. As a rule the hemorrhage soon stops. 
As the tissue becomes distended with blood and lymph the 
pressure becomes so great that further hemorrhage is 
mechanically lessened or prevented. Furthermore the 
destroyed cells liberate fibrin ferment which aids in coagula- 
tion of the blood, thus preventing fm'ther hemorrhage. 
Should the force strike an exposed part which already 
shows a blood infiltration, a progressive necrosis of the 
rather poorly nourished cells can easily take place. Seldom 
is the udder tissue alone affected, as usually the skin is in- 
volved at the same time and manifests superficial abrasions 
of the epidermis and swelling and blood infiltration of the 
corium and subcutaneous connective tissue. 

These alterations in the udder tissue then call forth 
an inflammation with emigration of leucocytes. This in- 

8 



MASTITIS CAUSED BY EXTERNAL FORCE 9 

flammation clears the tissue of extravasated blood and 
necrotic particles and fills the defects made in the tissue 
by necrosis and its resorption, with connective tissue. 

Similar phenomena occur in the skin as dermatitis 
when it becomes involved. 

Termination. — After resorption of the exudate in the 
inflamed area, more or less sclerosis remains followed by 
atrophy of the tubules. If the skin has also been involved 
in the inflammation, it is no longer movable but is firmly 
adhered to the udder. 

If there is a wound in the skin it may easily become 
infected. This infection can possibly reach the injured area 
in the udder through the lymph-vessels and in that way 
give rise to an infectious mastitis. 

Clinical Symptoms. — We see immediately or soon 
after the impact of the force, as a rule, the formation of a 
moderate circumscribed swelling which is the primary 
lesion. In the course of one day the swelling increases, be- 
comes hot (hypersemia), painful and somewhat firm fol- 
lowing blood coagulation and cellular infiltration. 

After several days the swelling begins to recede and 
gradually diminishes, after which, however, a somewhat 
firmer, more circumscribed nodular formed area remains, 
due to connective-tissue induration. 

Treatment. — The condition is not serious. Usually no 
treatment is necessary. The process heals out rapidly. 

In the first few days one can reduce the hypersemia and 
hemorrhage by the use of cold-water treatment (vaso- 
constriction) . One can apply a cold water compress to the 
udder by a suspensory bandage placed around the middle. 
If the skin is injured one can prevent infection of it by 
the use of a Burrow's solution compress. 

When the swelling begins to recede one can assist the 
treatment by the use of a skin irritant, as concentrated 
iodine solution rubbed in as a stimulation to resorption. 



10 MASTITIS OF THE COW 

WOUNDS OF THE UDDER 

Etiology. — Wounds of the udder may be produced by 
blows, or stabs as by a pitch- fork, hooking, or from a sur- 
gical operation such as an incision in an abscess. 

This brings us to the discrimination between the pri- 
mary lesion and the subsequent inflammation. 

The wound ruptures the vessels and milk passages, fol- 
lowing which the walls of the wound become infiltrated 
with blood, lymph and milk which flow outward through 
the mouth of the wound. The hemorrhage may be more 
or less copious. It is greatest following incisions and least 
in contused wounds, that is in wounds produced by dull 
objects, as a tlu'ust from a horn. In contused wounds the 
vessels of the neighborhood are so injured that thrombosis 
occurs in most of them. This prevents hemorrhage but 
predisposes to necrosis. 

Inflammation. — The reactive inflammation begins in 
the immediate vicinity of the wound, that is, the walls of 
the wound, where a wall of emigi-ating cells [j^hagocytes] 
is formed which clears the wound of dead tissue and foreign 
particles. Around this a connective-tissue wall is formed 
which closes the ruptured tubules and from which con- 
nective-tissue cells rapidly proliferate until the wound aper- 
ture is gradually filled with young succulent loose con- 
nective tissue, gi'anulation tissue. 

Termination. — In the most favorable cases the wound 
heals without any complication. The newly formed connec- 
tive tissue fills the wound aperture, and the surface is finally 
covered by regeneration of the epidermis from the margin 
of the wound. The exudate is resorbed and the loose con- 
nective tissue strongly contracts, finally leaving a white 
fibrous line or scar. 

As a rule, however, udder wounds become complicated 
with infection. In these conditions healing is usually de- 
layed, necrosis of the connective tissue is more widespread 



MASTITIS CAUSED BY EXTERNAL FORCE 11 

and not infrequently such a condition can develop into a 
more protracted exudative gangrene. 

Treatment. — Our treatment is to avoid an infection 
when possible and to check its progress when one has taken 
place. 

The wounds are thoroughly disinfected. In the begin- 
ning a Burrow's solution compress is applied to the udder 
( suspensory bandage ) . Infected wounds are freely opened 
so that the exudate may have free drainage, necrotic parts 
are removed, following which a scrupulous antiseptic treat- 
ment is carried out. 



CHAPTER IV 

INFECTIOUS MASTITIS IN GENERAL 

Ports of Infection 

The causes of infection may enter the udder: (a) 
through openings in the udder, and ( h ) through the blood- 
stream. 

The openings which may serve as ports of infection to 
the udder are of two different types : ( 1 ) natural : the teat 
canals, and (2) morbid: wounds. 

THE TEAT CANAL AS A PORT OF INFECTION 

Infectious material enters through the teat canal, so 
that first the milk and indirectly through it the tissue 
become infected. 

The milk is a nutritious fluid and contains water, salts, 
albumin, carbohydrates, and fats. It is an excellent source 
of nourishment for bacteria and therefore difficult to pre- 
serve, especially in summer, since it easily undergoes acid 
fermentation in vessels. 

The udder keeps the milk warm, like a thermostat, and 
offers very favorable conditions for bacterial development. 

Under normal conditions, however, the milk in the 
udder is practically sterile. The reasons for this are of 
two types: (a) physical nature, and (b) biological nature. 

Physiological causes of sterility of milk in the udder. 
The teat canal is closed between milkings by bundles of 
smooth muscle tissue imbedded in the walls which maintain 
a definite moderate tension. Thus under physiological 
conditions the external opening of the teat canal is small, 
usuallj^ rendering infection more difficult. 

Furthermore, the teat canal is directed downward, or to 
the side when the cow is lying, but never upward, as the 

12 



INFECTIOUS MASTITIS IN GENERAL 13 

dorsal position is not physiological to the cow. Thus 
usually the bacterial infection takes place in a direction 
opposite to that of gravitation, never in the direction with 
it, wliich usually is an obstacle to infection. 

Finally the milk stream passes only in one direction, 
outward from the udder through the teat canal by sucking 
or milking. A retrogressive stream does not occur. The 
udder is mechanically distended by the milk and collapses 
like an empty glove after milking, without the influence 
of any in-sucking force. Thus the infection must enter 
against the stream, never with it. 

Biological causes for sterility of milk in the udder. 
In spite of the before mentioned obstacles to infection one 
or more bacteria may gain entrance, but these may be taken 
up and destroyed by the ever-present leucocytes which are 
more or less numerous. The leucocytes play a very impor- 
tant part inasmuch as they inhibit the invasion of the 
milk by bacteria. [The normal healthy udder of the cow 
harbors bacteria throughout its whole extent (Ward). 
The healthy udder always gives milk which is entirely bac- 
teria free (Kitt., vol. i, 2d ed., p. 227).] 

Predisposing factors to infection through the teat 
canal. These factors are of two types: {a) physical nature, 
and ( b ) biological nature. 

Predisposing Causes of a Physical Nature. — Arrest of 
milk secretion is produced by neglecting to milk or from 
poorly regulated milking hours. For the same reasons 
the cisterns can become so distended with milk that the 
pressure finally overcomes the tension of the sphincter 
muscle and the teat canal fills with milk which continu- 
ously drops from the end of the teat. A rapidly growing 
or motile bacillus can now easily gain entrance against 
the stream, grow in the milk in the teat canal, and finally 
infect the entire milk. 

A paralysis of the sphincter muscle following age, as 



14 MASTITIS OF THE COW 

in old milch cows, or a more severe affection, as a chill or 
fever,^ causes the same alteration, and dilatation of the milk 
canal takes place and predisposes to infection. 

Infection may be induced by the introduction of in- 
struments, as a milk tube in the teat canal, or spontaneously 
with foreign bodies, as a straw which may be forced into 
the teat canal when the cow lies down. 

Predisposing Factors of a Biological Nature. — \Vlien 
a very virulent rapidly growing bacillus gains access to 
the mouth of the teat canal it can always find spaces in 
that passage containing moisture from the physiological 
capillaries in which it can grow. Through its own virulence 
it can withstand the leucocytes (negative chemotaxis) [ag- 
gressins], and infect the milk. This explains the distinctly 
contagious character of many cases of mastitis. 

Prophylactic Measures Against Infection Through the 
Teat Canal. — Avoid aiTest of the milk secretion by well- 
regulated milking hours and punctuality in milking. Use 
the milk tube cautiously. Keep the teats clean and dry. 
In cases of contagious mastitis isolate the diseased indi- 
vidual, milk it last and disinfect the morbid milk in order 
to avoid the possibility of spreading the infectious material 
in the cow stable. 

UDDER WOUNDS AS PORTS OF ENTRANCE 

Udder wounds may already be infected from the be- 
ginning, that is, the infectious material is injected at the 
same time that the wound is made. Such is often the case 
in stab wounds. In other cases a wound may be sterile 
at first and become infected later. 

In fresh wounds the exterior of the wound itself and 
also the milk through the ruptured tubules may become 

^ Both appear to be followed by paresis of the involuntary 
muscles which among other things produces diminished peristaltic 
action. 



INFECTIOUS MASTITIS IN GENERAL 15 

infected. In old wounds tliis is prevented by the inflam- 
matory connective-tissue formation. 

Protection of Wounds Against Infection. — The 
leucocytic wall forms the most important protection against 
infection of the wound. But since the wall of leucocytes 
is only an evidence of inflammation, that process plays 
a very important part against infection. 

Finally the inflammatory connective-tissue wall forms 
a very good obstacle to the progress of infection, as it 
circumscribes it. 

Predisposing Factors to the Infection. — The nutrient 
fluids, blood, lymph, and milk which infiltrate the udder 
wound, predispose it to infection more than any other 
wound because of the favorable nutrient conditions for the 
infectious organisms and because the wound itself is a 
good thermostat. 

The greater the blood infiltration, the more widespread 
the death of cells, and the more saturated with fluids the 
wound is, just so much better it is for infection. It is 
broken down by the bacteria which as a rule live more 
easily on dead than on living media. In the latter case 
they are more directly exposed to healthy phagocytes. 

THE BLOOD AS A PORT OF INFECTION 

In order that the blood coming into the udder may be a 
port of infection, it is necessary that we have a blood-infec- 
tion, that is, that the infectious organisms be in the blood 
stream. 

Blood-infection. — The blood can become entirely or 
partially infected, that is, general blood-infection (bac- 
tersemia), or partial blood-infection. 

A partial blood-infection is possible in this way, that 
the infectious organism be deposited in the organs or be 
transported to the organs from the blood by leucocyies. 



16 MASTITIS OF THE COW 

The local blood-infection, which is of importance to the 
udder, is through infection of the blood of the aorta. 

Causes. — A blood-infection can be produced in differ- 
ent ways. Infectious material may be picked up by the 
leucocytes in an infected area in the intestines or in other 
organs rich in bacteria and be carried by them into the blood 
stream. In a wound infectious organisms can grow di- 
rectly in ruptured vessels. In the infection of an organ the 
primarj" lesion (necrosis) may become permeated with in- 
fectious organisms, which surround the vessels of the pri- 
mary lesion, inducing deep necrosis, so that a blood-infec- 
tion may take place through the walls of these vessels. 
Blood-infection can be induced through infectious ulcera- 
tion of a vessel wall. Should the lymph become infected 
(lymph-infection) this fluid can finally infect the blood. 

The usual causes of infection of the blood of the aorta 
is a lung-infection or an infectious endocarditis. 

If the blood of other organs, for instance of a wound or 
of a uterus, as in infectious metritis, be infected the blood 
of the aorta can still remain sterile, since the infectious 
material is filtered out in the lungs. This is the rule for 
infectious organisms of positive chemotaxic action, while 
on the contrary infectious organisms of negative chemo- 
taxic action easily pass through the lungs. 

With infectious pnemnonia usually a blood-infection 
is brought about thi-ough ulceration of a vein wall with 
emptying of infectious fluid material into the blood of 
the veins. 

The exudate discharges itself into the vein gradually 
and thus divides itself minutely. It becomes further com- 
minuted in its passage in the vessel by impact against the 
vessel wall, and through the action of the current eddies in 
the vessel ramifications. A drop of exudate discharged 
into the vein can become so finely divided in this way that 
it can be distributed over an incredibly large area. 



INFECTIOUS MASTITIS IN GENERAL 17 

Infection of the blood stream is not of long duration 
as the blood soon deposits the infectious organisms and 
thus purifies itself again. Infection of the blood can recur, 
however. 

An acute fatal general blood-infection like anthrax 
naturally cannot give rise to a local diseased process, such 
as inflammation of the udder. A non-fatal generalized 
blood-infection can, however, produce different infectious 
local disease processes, such as pneumonia, pleurisy, arthri- 
tis, nephritis, and perhaps mastitis. 

Infection of the Blood of the Udder. — The possibility 
of one of these emboli reaching the udder is very great, since 
both external pudic arteries are fairly large, have no im- 
portant curves, and are incipient at the aorta. [External 
iliac, femoral artery, external pudic or mammary artery.] 

As the aorta runs on the left side [anterior part], the 
most direct course is to the left half of the udder which is 
therefore most exposed to a blood-infection. It is clear, 
however, that the situation and the time during which the 
emboli are passing in the blood are of great importance. 
If, for instance, a cow stands with her posterior extremity 
inclined toward the left, the right external pudic artery is 
the most direct course. For the emboli to reach the pos- 
terior quarters the most direct way seems to be through 
the external pudic arteries. 

Thus the left quarters of the udder are more exposed 
to a blood-infection than the right, and the posterior quar- 
ters more so than the anterior. The left posterior quarter 
therefore is the most severely exposed. 

The small infectious emboli, if they be sufficiently large, 
may be caught in the capillaries or fine arterioles and at 
these points produce a thrombus with infectious necrosis 
and the formation of infectious metastatic foci. In other 
cases very small emboli may be taken up and carried into 
the loose intralobular connective tissue where the leucocytes 

2 



18 IVIASTITIS OF THE COW 

degenerate, remain and die when the infectious organisms 
are the stronger. Here a metastatic infectious focus is 
produced. On the other hand, if the leucocytes are the 
stronger, the infectious organisms are destroyed without 
the production of tissue alterations. 

In tliis manner, as a rule, through infection by the blood 
to the udder a great number of small foci, distributed 
throughout the connective-tissue stroma of the udder, are 
formed. 

Infection of the Udder in General 

The infection of the udder may be divided - into milk' 
infection and stroma-infection, depending upon the posi- 
tion of the infectious organisms. 

milk-infection [Parenchymatous Mastitis] . 

Definition. — Milk- or parenchyma-infection is an in- 
fection of the udder in which the bacteria are only found 
in the milk, or rather in the parenchymatous passages. 

Since the parenchymatous tubular system of one quar- 
ter does not connect with that of the other quarter the con- 
dition remains confined to the quarter infected. 

Ports of Infection. — The milk-infection [paren- 
chymatous mastitis] may be primary or secondary. 

The primary milk-infection is produced by infection 
through the teat canal or through a ruptured tubule in a 
fresh wound. 

The secondary milk-infection is a subsequence of 
stroma-infection [interstitial mastitis] with extension of 
an infectious focus in the stroma to a milk passage, ulcera- 
tion through the wall of the tubule and into the milk tubule. 

Milk-infection causes a local condition in the udder as 
well as general conditions. 

^ I have made this division, since it appears to me better than 
the old divisions indicated by the position of the disease. 



INFECTIOUS MASTITIS IN GENERAL 19 

The Local Condition. — We must here distin- 
guish between the primary lesion and the subsequent 
inflammation. 

Primary Lesion. — ^We distinguish between the quan- 
tity or extent, and the quality or character of the primary 
lesion. 

Quantity. — The primary lesion may be more or less 
extensive. It may be circumscribed upon a greater or 
smaller part of a quarter of the udder or it may be diffusely 
spread over the entire quarter. 

Naturally it always begins by affecting a localized part 
but can become diffuse through spreading of the infectious 
organisms in a comparatively short time (a few hours, 
days or weeks ) . 

The factors which may circumscribe the infection are 
mechanical or biological in character. 

The mechanical inhibiting influences are the milk stream 
and gravity. The infectious organisms must develop 
against the current of the milk secretion, which is usually 
a fairly effective obstacle to an extension of the infection. 
Greater difficulty is experienced by the infectious organ- 
isms in developing in the milk-ducts in the opposite direc- 
tion to gravity. For this reason, therefore, they grow at 
first in the horizontal milk passages on either side of the 
teat bases, especially in the part behind the teats of the pos- 
terior quarters and before the teats of the anterior quarters. 
The progress upward is more difficult and more protracted. 

The inhibiting biological influences against the bacteria 
are the leucocytes. 

If the organisms grow slowly phagocytosis usually pre- 
vents spreading of the infection. 

The primary lesion more or less quickly produces an 
inflammation in the region, with emigi-ation of leucocytes 
which may mechanically prevent further infection. It cre- 
ates a cell stopper against the infection, as it were. 



20 



IVIASTITIS OF THE COW 



These factors adequately support each other, that is, a 
localized primary lesion is caused by an organism of low 
virulence . and slow growth, while, on the other hand, 
the diffuse primary lesion is caused by an organism 
of high virulence and rapid growth. When the viru- 
lence is extremely high inflammation may be retarded or 
prevented. 

Quality. — The alterations in the primary lesion are of 
a retrogressive type, and are usually of degenerative or 
necrotic character. These retrogressive 
changes, however, may vary in degree. 
In the mildest cases they may consist 
only of degeneration of the epithelium. 
The epithelium may however become 
necrotic and a croupous membrane form. 
If the connective tissue becomes necrotic 




Fia. 3. — Milk - infection 

LPuXtry^sis^'^'se^^^^^^ a deep diphtheritic membrane is pro- 

primary lesion, with diffuse 
gangrene (150). Nuclei in- 
distinctly or not at all stained 
due to necrosis. The intra- 
lobular connective tissue is 
distended with red blood 
cells following hemorrhage. 
The tubules are compressed 
anil contain desquamated 
epithelial cells. Numerous 
staphylococci were demon- 
strated in the tubules by 
using bacterial stains. 



duced. Greater portions of the udder 
may become necrotic, as the single tu- 
bules, or groups of these tubules, form- 
ing nodular necrosis. The entire part 
of the udder affected may rapidly be- 
come necrotic or develop into diffuse 
gangrene (Fig. 3 ) . 
The quantity and quality of the primary lesion depend 
upon the character of the infectious organism and the con- 
dition of the udder. The more virulent the organism, the 
greater is the area and the more severe the character of the 
primary lesion. 

Organisms of the same virulence however produce a 
greater primary lesion after parturition than during the 
gestation period. Under identical conditions, that is, the 
same virulence of organisms and same time after parturi- 
tion, the primary lesion is greater in good milch cows than 
in those that are poor milkers. These circumstances are 



INFECTIOUS MASTITIS IN GENERAL 



21 




dependent upon the quantity of milk, which is great in one 
case and small in the other, and thus provides a more or 
less favorable condition for existence for the bacteria. 

The milk is also changed by the primary lesion. The 
more widespread and severe the alteration in the udder 
the greater are the changes in the milk. The casein and 
fat content of the milk is lessened by degeneration of the 
parenchymatous cells. The milk is rich in albumin in con- 
sequence of transudation from the blood stream, shows an 
increase in cells following desquamation 
of necrotic epithelium and is of a red 
color due to retrogressive metamorphosis 
of the red blood corpuscles. 

The inflammation occurs as a reac- 
tion to the primary lesion. 

Since the infectious organisms lie in 
the tubuli, quantities of leucoc}i;es wan- 
der into the lumen of those structures. 
The milk is therefore rich in cells ( Fig. 4 ) . 

Quantity. — If the primary lesion is 
circumscribed, the inflammation is cir- 
cumscribed, and if the primary lesion 
is diffuse, the inflammation is likewise 
difl'use. (Except in difl*use necrosis. 
See later. ) 

Quality. — The exudate is of a suppurative purulent 
character. The inflammation, following the character of 
the primary lesion, is purulent catarrhal, purulent croupous, 
or diphtheritic, sequestrating or apostematous. 

The more virulent the infectious organism the longer 

the inception of the inflammation is deferred, and thus the 

greater the primary lesion will be. The strongly virulent 

infectious organism works repellently upon the leucocytes 

(negative chemotaxis). 

The necrosis produced by the infectious organism how- 



Fio. 4. — Milk-infection 
[parenchymatous mastitis) 
Colibacillosis. Acute in- 
flammation (X 150). The 
epithelial ceils are swollen 
and show weak nuclear 
staining (degeneration). 
At a few places there are 
a few layers of cells. In- 
tense cell infiltration in 
the intralobular connec- 
tive tissue and severe emi- 
gration of cells into the 
tubules. A few colon ba- 
cilli were seen in the 
tubules by using bacterial 
etaina. 



22 MASTITIS OF THE COW 

ever mechanically hinders this repulsion, and the necrosis 
also prevents a strong attraction for the leucocytes. In 
defence of the body the leucocytes are finally attracted to 
the necrosis, and now the infectious organisms are sub- 
jected to the action of these cells which inliibit their growth 
and toxin production. The weakened infectious organisms 
can then be rendered innocuous or killed or be dislodged 
with the necrotic masses and be discharged with the milk. 

Through desquamation of a necrotic, croupous or diph- 
theritic membrane a milk-infection can develop into a sec- 
ondary stroma-infection. Following such desquamation a 
wound is formed which can become infected (wound- 
infection. ) In this manner a sequestrating puinilent inflam- 
mation with nodular necrosis is produced, constituting a 
secondary stroma-infection or interstitial mastitis. Fol- 
lowing complete softening of the sequesters the area is 
changed into an abscess with a thick fibrous wall, which is 
produced by inflammatory proliferation of the adjacent 
connective tissue. 

In diffuse necrosis mastitis as a sequestrating inflam- 
mation naturally cannot proceed further than the periph- 
ery of the diseased quarter of the udder. 

Milk. — The milk, which is changed by the primary 
lesion, is further altered by the inflammation. It is ex- 
tremely rich in cells and therefore purulent, thick and 
pulpy. Its color is yellowish-gray, due to the presence of 
cells, and it often contains croupous membranes as thick 
yellow shreds. The reaction is somewhat strongly alkaline. 
The milk never contains clumps of casein. [Kitt and 
Jensen describe casein clumps in morbid milk.] 

Complication with Saprophytic Invasion. — Under 
the usual conditions pathogenic bacteria, but not sapro- 
phytes, may invade the milk in the udder. If the latter 
do gain entrance they are taken up by the leucocytes and 
destroyed. It may be different in other conditions such as 



INFECTIOUS MASTITIS IN GENERAL 23 

an udder-infection. The leucocytes which are dangerous 
to the saprophytes may be called back by the patho- 
genic organisms, and then the saprophytes may develop 
unhindered. 

They cannot attack living tissue, but the necrosis pro- 
duced in the primary lesion constitutes an excellent culture 
medium for them, and consequently undergoes putrefac- 
tion. We may call this process exudative gangrene.^ 

These saprophytes are large, anaerobic, rod-shaped 
putrefactive bacteria. 

A saprophytic invasion of this type may easily occur 
in croupous mastitis, since a shred of fibrin can remain 
hanging in a teat canal. A shred of this kind can then 
become permeated by saprophytes which grow in and 
through it, so that the shred may constitute a good bridge 
for the infection. 

Following such a saprophytic invasion with exudative 
gangrene, the milk becomes stinking, homogeneous and 
thinly fluid, since the necrotic cells and the fibrin shreds 
dissolve during putrefaction, and the leucocytes are killed 
by the poisons of putrefaction. 

GENERAL CONDITIONS 

Blood-infection. — The primary lesion may be per- 
meated with the growing pathogenic organisms, which 
induce deep necrosis with destruction of the blood-vessel 
walls, so that the bacteria may enter the vessel and produce 
a generalized blood-infection or septicaemia. This second- 
ary blood-infection, if not overcome by the defensive ele- 
ments of the blood, can induce secondary lesions, as an in- 
fectious pneumonia or arthritis. 

Death caused by an acute general blood-infection is 
due to septic intoxication. The external symptoms of a 

^ These necrotic parts will be thrown off with the croupous 
or diphtheritic exudate and constitute a part of that exudate. 



24 MASTITIS OF THE COW 

general blood-infection or bactereeniia are the same as in 
the septic intoxication. 

Intoxication. — From the diseased quarter of the 
udder a stream called the exudative stream passes into 
the milk, and another stream called the resorption stream 
passes into the blood. 

This resorption stream carries a quantity of toxin 
produced by the infectious organisms, which induces the 
more or less distinct appearance of intoxication, which we 
call septic intoxication because it is caused by infectious 
material or the toxins of , pathogenic bacteria. 

Septic intoxication presents a collection of general or 
nervous symptoms which we call fever symptoms [complex 
symptom of fever] . They are : 

1. The heart shows an increase in the frequency but 
a decrease in the force of the beat. 

2. Respiration shows an increase in frequency but a 
decrease in volume (dyspnoea) . 

3. The skin is warm, due to hypereemia following vaso- 
dilation. 

4. The voluntary muscle shows diminution of power 
[trembling, decubitus] . 

5. The smooth muscle likewise shows a diminution of 
power. Peristalsis is especially weakened or ceases en- 
tirely, inducing indigestion or impaction. [It may alter- 
nate with increased activity and diarrhoea.] 

6. The secretion of sweat is more or less increased. 

7. The body temperature is increased. [It may be 
normal or decreased.] 

8. Consciousness is diminished. 

Fever begins however with a stage showing the oppo- 
site symptoms, which resemble the reflexes produced 
through stimulation due to irritation by cold. The clonic- 
tonic spasms of the voluntary muscles called shivering, 
are very prominent, likewise the coldness of the skin due 



INFECTIOUS MASTITIS IN GENERAL 25 

to ansemia of the skin following vasoconstriction [chill]. 
In this stage the body temperature ascends as a result of 
increased heat production by muscle spasms and the di- 
minished heat radiation due to anaemia of the skin. [Visce- 
ral congestion, retention of waste products, and increased 
retrogressive cellular metabolism also play a part in heat 
production.] 

In consequence of the high temperature and the great 
heat loss through hypersemia of the skin, combustion and 
consumption of energy are very great in fever. 

Death may be produced in septic intoxication by paraly- 
sis of the heart or the vital nerve centres by the effect 
of toxins. 

In exudative gangrene a putrid toxin or putrefactive 
poison [cadaverin] is formed which produces putrid intoxi- 
cation when resorbed. An intoxication of this kind is 
called septic-putrid intoxication [septico-sapremia]. 

Putrid intoxication also presents symptoms of fever. 
Death may easily occur in this condition, and it is pro- 
duced with distinct paralysis of the nerve centres, indicated 
by collapse, with subnormal temperature, muscular paraly- 
sis, and loss of consciousness (narcosis). 

Termination. — Milk-infection or parenchymatous 
mastitis is seldom fatal. The cause of death is septic or 
septic-putrid intoxication. 

This general intoxication can, however, usually reduce 
the milk secretion and nutritive condition of the animal. 

The udder can heal after desquamation and removal 
of the necrotic parts. Healing takes place with loss of 
substance which is principally replaced by connective tis- 
sue with atrophy of the milk-producing parenchyma. 

The duration of the condition depends upon the quan- 
tity and quality of the primary lesion and may be from four 
days to one month or even longer, as is the case in nodular 
necrosis. 



«6 MASTITIS OF THE COW 

Not infrequently, however, the infection is progressive 
in spite of the inflammation. The infection spreads fur- 
ther to the healthy lobuli and induces a new primary lesion 
with its subsequent inflammatory reaction. 

The course therefore is more protracted. The condition 
may last from a month to a year and the terminal result 
is a diffuse sclerosis and atrophy of the parenchyma. 

The functional capacity of the udder becomes more or 
less reduced following the inflammatory process induced 
by the milk-infection. This deficiency may be overcome, 
however, through vicarious hypertrophy of the unaltered 
parts of the udder. 

STROMA-iNFECTiON [Interstitial Mastitis'] 

Definition. — Stroma-infection or interstitial mastitis 
is that infection of the udder in which the infectious or- 
ganisms are only found in the stroma or interstitial con- 
nective tissue. 

The pathogenic organisms invade the lymph spaces of 
the intralobular connective tissue. 

Since the connective-tissue system binds the different 
quarters of the udder together, the stroma-infection can 
spread from one place to the neighboring tissue, while the 
milk-infection, on the other hand, is confined to the infected 
quarter. 

The stroma-infection may be divided into two principal 
groups : 

1. Stroma-infection of an acute character. 

2. Stroma-infection of a chronic character. 
Stroma-infection of an Acute Character [Acute 

Interstitial 31 ostitis]. — These cases depend upon quickly 
acting infectious organisms, which in their active way may 
produce an acute, never typically chronic, process. 

The point of infection is one or more wounds. The 
blood is seldom the source of infection and this infection 



INFECTIOUS MASTITIS IN GENERAL 27 

in the udder may be primary in the stroma, although not 
coming from the milk into the stroma. The wound is 
caused by an external violence and is therefore an external 
wound which opens through the skin. The pathogenic 
organisms come into the wound from the exterior. The 
infection through the blood, due to its position in the udder, 
is always primary in the stroma. 

Furthermore, this infection can be secondary in the 
stroma when it comes into the stroma from the milk. The 
wound, or the wounds, are caused by milk-infection with 
development of necrosis after the occurrence of desquama- 
tion or secondary wounds. These internal wounds are in- 
fected by the same infectious organisms which cause the 
milk-infection [parenchymatous mastitis]. 

The location of the bacteria in these stroma-infections 
is in the wound secretions and in the primary lesion. 

Local Condition. — The primary lesion extends over 
the surface of the wound and forms a superficial or more 
or less deep necrosis. The wound secretion is usually 
altered by the primary lesion. Following the necrosis of 
the vessels the lymph or plasma extravasation increases, 
the blood corpuscles remain for the most part in the vessels. 
The secretion is colored red by haemoglobin due to necrosis 
of red corpuscles. 

In stroma-infection, through the blood, more frequently 
larger or smaller embolic areas of necrosis are found. 

The inflammation induces a severe leucocytic emigra- 
tion into the connective tissue of the walls of the wound 
and into the wound. The wound secretion is suppurative. 
It contains a great quantity of cells, leucocytes and young- 
connective cells, has a gray or yellowish-gray color and is 
somewhat thick. 

Around the necrotic parts a dissecting cell-ring of leu- 
cocytes forms, which loosens the necrosis. 

The loosened necrotic material can slough directly to 



28 MASTITIS OF THE COW 

the exterior in external wounds, or in internal wounds be 
forced or desquamated toward the interior into the milk. 

In nodular necrosis following milk-infection or in em- 
bolic necrosis following infection through the blood, the 
necrotic material cannot be gotten rid of as such, but it can 
be liquefied through the action of the infectious organisms 
and the cells of the inflammation (so-called suppurative 
softening). The pus formed in this manner can empty 
itself through the milk passages (in which the primary 
embolic stroma-infection thus induces a secondary milk- 
infection) or directly to the exterior through ulceration of 
the skin. The latter, ulceration of the skin, occurs how- 
ever only in superficial nodules. In other cases complete 
or only partially liquefied areas of necrosis can become 
encapsulated following a stronger proliferation of periph- 
eral connective tissue. This condition is then chronic. 

The Milk. — In externally infected wounds which have 
not progressed to a milk-infection, the milk is only slightly 
or not at all altered. The quantity, however, is more or 
less diminished. 

In internally infected wounds the milk possesses the 
same character as in the milk-infection [parenchymatous 
mastitis]. 

A complication with saprophytic invasion can occur and 
develop into an exudative gangrene. The exudate is stink- 
ing and less densely fluid. 

Blood-infection. — Bacteremia. — In addition to en- 
tering the milk, infectious organisms of a high virulence can 
enter the blood stream through the opened blood-vessels 
of a fresh wound or through the walls of the vessels injured 
in the primary lesion. In thLs manner an acute blood- 
infection can take place, which, if not fatal, leads to sub- 
sequent disease processes as infectious pneumonia or 
arthritis. 

Intoxication. — Stroma-infection can also result in 



INFECTIOUS MASTITIS IN GENERAL 29 

septic intoxication, or develop into exudative gangrene 
and then septic-putrid intoxication with the same symptoms 
as before described, and these conditions may terminate 
in death. 

Termination. — Stroma-infection or interstitial mas- 
titis very seldom terminates in death. Healing is the rule. 
The wounds heal after sloughing of the necrotic parts, with 
more or less sclerosis and parenchymatous atrophy. 

Nodular necrosis following milk-infection or the less 
frequent embolic necrosis may form chronic wounds which 
may induce a sort of relative healing through encapsulation. 

Stroma-infection of Chronic Character [Chronic 
Interstitial Mastitis^. — The action of the bacteria is of 
a chronic progressive character. 

Ports of Infection. — These infections may take place 
through the teat canal, through wounds or through the 
blood stream. 

In the latter case the infection is always primary in the 
stroma due to its position in the udder. Whatever the 
port of entrance may be the organisms are taken up by 
the leucocytes and carried into the IjTnph spaces of the 
stroma. Here the leucocytes soon become paralyzed and 
are necrotized by the bacteria. 

Local Conditions. — The primary lesion consists of 
many single spreading areas of necrosis in the stroma 
around the point of infection in the teat canal, wound or 
at the point of infection from the blood stream. 

Around each primary lesion the inflammation produces 
a strong ring of leucocytes and outside of this a wall of 
new- formed connective tissue. 

Thus the inflammation produces many small areas or 
nodules the size of a pin's head or smaller (Fig. 5) . 

The progressive character, that is, the chronic enlarge- 
ment of the primary lesion, the necrosis, is diagnostic of 
this infection. The primary lesion is chronic, as it were. 



30 



MASTITIS OF THE COW 




and usually is not circumscribed by an inflammation. The 
necrosis develops slowly at its periphery through necrosis 
of the cell wall. This cell wall around the spreading area 
of necrosis, however, is maintained by proliferation of new 
connective-tissue cells. In this manner the nodules develop 
and become the size of hemp seed or larger. 

Following this development of the lesions many adja- 
cent areas of necrosis may coalesce and finally produce 
great necrotic nodules the size of a hen's egg. 

The infectious organisms may be picked up by the 
leucocytes and carried into the lymph 
spaces of the stroma inducing the for- 
mation of the new areas of necrosis or 
daughter nodules. 

The necrotic nodules may open a 
milk-duct and thus induce a secondary 
milk-infection [parenchymatous mas- 
titis]. In the same way, but less fre- 
quently, they may open the skin by 
ulceration and cause fistulae. 

Because of their position in the stro- 
ma the nodules compress the tubules 
and produce pressure atrophy of their 
cells. The milk is most altered in quan- 
tity which is decreased more or less. The composition is 
less changed. The fat content lessened. It is poor milk. 
Complication by saprophytic invasion is rendered im- 
possible. It is closed off by a completely circumscribing 
wall of connective-tissue cells. 

If a secondary milk-infection is produced by ulceration 
of a milk-duct or a fistula formed by ulceration of the skin, 
saprophytic invasion with its subsequent putrid softening 
is possible through the openings in the necrotic areas in 
the stroma. 



Fig. 5. — Stroma-infec- 
tion [interstitial maBtitis] 
of chronic character. Pyo- 
bacillosia (150). Two 
groups of cells (emigration) 
are \-isible in the swollen 
cellular intralobular con- 
nective tissue. The tu- 
bules are compressed. In 
one tubule a few cells are 
present. By the use of 
bacterial stains a few bac- 
teria, pyogenes bacilli, were 
demonstrated in the centre 
of the cellular foci. 



INFECTIOUS MASTITIS IN GENERAL 31 

A usual obstacle to such saprophytic invasion, however, 
is the fact that the organisms which produce the necrosis 
have a strong attraction for leucocytes. Thus these cells 
are present in great numbers and rapidly pick up and 
destroy the saprophytic bacteria. Saprophytic invasion 
is prevented in this manner. 

If, on the other hand, the leucocytes in a secondary in- 
fection are repelled by a very strongly virulent infectious 
organism, a saprophytic invasion is possible and in fact 
usual. 

GENERAL CONDITIONS 

Blood - infection. — A blood-infection can occur 
through ulceration of a vein and through lymph-infection. 
Since the infectious organisms exert a strong attraction 
upon the leucocytes the blood is soon cleansed by phagocy- 
tosis. The organisms are transported to the lung tissue 
where secondary metastatic foci may be formed. 

Intoxication. — The stroma-infection concerned pro- 
gi-esses to a chronic septic-intoxication with indistinct fever 
symptoms as a rule. It induces a chronic progressive in- 
appetency and emaciation which finally terminates in death. 

An unimportant but apparent change is the thickening 
of the skin (sclerosis) with a rough hair coat. This altera- 
tion is probably caused by the direct action of the toxin. 

If gangrene be added the intoxication is septic-putrid. 
The fever is more pronounced and death may be induced 
in a somewhat acute manner. 

Termination. — This type of stroma-infection develops 
into a chronic progressive destruction of the udder, which 
can endure for a year. Furthermore it advances to a pro- 
gressive intoxication with emaciation which can terminate 
in death. 



32 MASTITIS OF THE COW 

Summary 

I. Ports of infection. 

A. Infection through openings in the udder. 

1. Natural openings: the teat canal. 

The milk as a natural culture medium for bac- 
teria. 
The causes of sterility of milk in the udder. 

A. Physical nature. 

The end opening of the teat canal. 
The direction of the milk canals. 
The milk stream. 

B. Biological nature : the leucocytes. 

The predisposing factors for infection through 
the teat canal are: 
AA. Physical nature. 

Arrest of milk secretion. 
Relaxed musculature. 
Infection with milk tubes and 
other foreign bodies. 
BB. Biological nature: virulent infec- 
tious organisms. 
Prophylaxis. 

Milking time. 
Cleanliness. 

Isolation of animals with contagious 
mastitis. 

2. Artificial openings : udder wounds. 

Defence of wounds against infection : the cell 

wall, the inflammation. 
Predisposing factors to infection of the wound. 
Blood infiltration and necrosis. 

B. Infection by the blood stream. 

Hypothesis : blood-infection. 
Causes of blood-infection. 
Infection of the udder-blood. 
Occurs, 

In the most strongly exposed parts of the udder, 

formation of metastatic nodules. 



INFECTIOUS MASTITIS IN GENERAL 33 

II. Udder-infection in general. 
A. Milk-infection. 
Definition. 
Ports of infection: primary milk-infection, infection 

through the teat canal or through wounds. 
Secondary milk-infection is one following stroma in- 
fection. 
1. Local conditions. 

A. Primary lesion. 

Quantity: circumscribed or diffuse. 

Circumscribing factors of a physical and 
biological nature. 
Quality: Superficial necrosis. 

Deep necrosis. 

Nodular necrosis. 

Diffuse necrosis. 
Alterations of the milk. 

B. Inflammation. 

Quantity: circumscribed, diffuse. 
Quality : catarrhal-purulent. 
Croupous-purulent. 
Sequestrating-purulent. 
Alterations of the milk. 
Complication Avith saprophytic invasion. 
Alterations of the milk. 
2. General conditions. 

A. Blood-infection. 

B. Intoxication. 

Septic-intoxication. 
Septic-putrid intoxication. 
Termination : relative health : seldom death. 
B. Stroma-infection. 
Definition. 

1. Stroma-infection of an acute character. 
Ports of infection. 

Primary stroma-infection : wounds, seldom blood- 
infection ; secondary stroma-infection : internal 
wounds following a milk-infection. 



34 MASTITIS OF THE COW 

A. Local conditions. 

Primary lesion. 

Inflammation. 

Sequestration and necrosis. 

Sloughing, softening, encapsulation. 

The milk. 

Complication with saprophytic invasion. 

B. General conditions. 

Blood-infection. 
Intoxication. 
Termination. 
2. Stroma-infection of a chronic character. 

Ports of infection : teat canal, wound or blood. 
Transportation of infectious organisms by leuco- 
cytes. 

A. Local conditions. 

Primary lesion. 

Inflammation. 

Distribution of progressive necrosis by the 

leucocytes. 
Secondary milk-infection, fistula formation. 
Milk. 

Complication with saprophytic invasion. 
Causes of its infrequent occurrence. 

B. General conditions. 

AA. Blood-infection. 

BB. Intoxication. 

Chronic septic-intoxication. 
Septic-putrid intoxication. 
Termination : progressive destruction 
of the udder. 

The milk-infection and stroma-infection apparently originate 
together very infrequently, however, as in an acute wound infection. 

As a rule they are very sharply separated originally, but may 
later complicate each other. 

Milk-infection often becomes complicated with the stroma- 
infection, which as a rule is less distinct, but as in nodular necrosis 



INFECTIOUS MASTITIS IN GENERAL 35 

may become more discernible. Chronic stroma-infection, like- 
wise, becomes complicated with a milk-infection which is indistinct 
at first but later becomes very severe and pronounced. 

The acute primary stroma-infection due to external uddcr- 
wounds, however, runs its course without complication, if it does 
not pass into a milk-infection in the beginning. 

The primary milk-infection is the most common, next comes the 
chronic stroma-infection. The primary acute stroma-infection is 
comparatively uncommon because of the important port of infec- 
tion, the udder-wound. 



CHAPTER V 

TYPES OF INFECTION 

Udder-infections may be divided primarily into two 
groups, depending upon the types of infectious organisms : 
(1) simple or single infection; (2) complex or mixed 
infection. 

Simple Udder-infection. — The simple udder-infection 
is caused by one kind of bacteria. 

There are, however, different kinds of simple infections 
because the type of organism which causes one case of 
simple infection may be of a different type in other cases 
of the simple infection. 

These types of infection induced by the different types 
of bacteria are divided into two classes : 

1. That type of infection which principally shows typi- 
cal milk-infection and externally only stroma-infection of 
an acute character. 

2. That type of infection which shows a typical stroma- 
infection of a chronic character. 

Types of Infection Which Shorn Principally Milk- 
infection or Externally Only Stroma-infection of an Acute 
Character. — These infections may be caused by three dif- 
ferent kinds of bacteria: (a) bacteria of the streptococcic 
group, streptococci; (h) bacteria of the staphylococcic 
group, staphylococci, and (c) bacteria of the colon group, 
colon bacteria or colon bacilli. 

The disease is named after the type of organism: Strep- 
tomycosis mamma?, staphylomycosis mammae, and coliba- 
cillosis mammas, or udder-streptomycosis, udder-staphylo- 
mycosis and udder-colibacillosis. 

Types of Infection Which Show Typical Stroma-infec- 
tion of a Chronic Character. — (a) Bacillus pyogenes; (h) 

36 



TYPES OF INFECTION 37 

the tubercle bacillus ; (c) the actinomyces fungus ; {d) the 
necrosis bacillus. 

They are named after the organism causing the infec- 
tion: Pyobacillosis mamma?, tuberculosis mammae, actino- 
mycosis mammae, and necrobacillosis mammae, or udder- 
pyobacillosis, udder- tuberculosis, udder-actinomycosis, and 
udder-necrobacillosis. 

Complex Udder-infection or Mixed Infection. — 
The mixed infection is caused by two or more types of 
bacteria. 

The bacteria which cause this disease are of the same 
type that cause the simple infection. 

The mixed infection may start originally as a primary 
mixed infection. 

Usually, however, it is .originally a simple infection and 
becomes complex or mixed later through secondary infec- 
tion (secondary milk-infection). 



CHAPTER VI 

UDDER-STREPTOM YCOSIS ( STREPTOCOCCIC 
MASTITIS) 

The infectious organism is one or more of the strep- 
tococcic group of pathogenic type. 

Character. — The pathogenic streptococcus is a small 
egg- or spherical-shaped organism which occm*s regularly 
as a chain of two or more individuals joined together. 
It is easily stained with the conmion anilin dyes and also 
w^ith Gram's method. The cultures are light or thin on 
the usual cultural media, especially surface growths. Gela- 
tin and milk are imaltered. 

The last characteristic, the condition of the milk, 
sharply differentiates the pathogenic streptococci from the 
non-pathogenic lactic acid streptococcus, which is found in 
milk, and which resembles the pathogenic streptococcus to 
such a great extent culturally and morphologically. 

There are names for the different types of pathogenic 
streptococci, as diplococcus pneumonije and streptococcus 
pyogenes, both found in man, streptococcus equi and Schutz 
diplococcus, both in the horse, and also the streptococcus 
mastitidis found in the cow.^ 

These groups of streptococci are differentiated princi- 
pally through their various sources. Otherwise they show 
very little morphological and biological difference. It is 
clear that the place in which the organism was found, its 
source, is no authentic and definite type characteristic, and 

* The galactococcus fulvus and galactococcus versicolor iso- 
lated from mastitic milk by Guillebeau certainly belong to the 
streptococcic group, while the galactococcus albus, which was only 
once isolated by Guillebeau, perhaps belongs with the micrococcus 
tetragenus (sarcina tctragena, Lehmann and Neumann). 
38 



UDDER-STREPTOMYCOSIS 39 

the appearance of the pathogenic streptococcus changes 
considerably under different conditions and therefore pre- 
sents less effective type characteristics. Special diagnostic 
type characteristics are not known. For a practical bac- 
teriological classification of the pathogenic streptococci we 
must wait for further work to be done. [Blake, The Classi- 
fication of Streptococci, Journal of Medical Research, 
March, 1917.] 

Occurrence. — The pathogenic streptococcus is not 
confined to any special geographical district but appears 
to be somewhat uniformly distributed. In Sweden it occurs 
throughout the entire country. Its occurrence is general. 
The frequency of the infection, especially the wound-infec- 
tion, indicates that it often occurs in the dust, in the soil 
of the cow stalls, and in the excrement. 

Morphology. — The pathogenic streptococcus presents 
variations in size. The greatest diameter can vary from 
0.9 to 2.3 micra. These are dwarf to giant forms. Usually, 
however, the greatest diameter is about 1 micron. 

The form as a rule is eg^- or lancet-shaped, seldom 
regularly round like a ball. Frequently the egg forms are 
so affected that they resemble rod-shaped organisms. 

As above stated, the individuals form chains. The num- 
ber of individuals in each chain is variable. In animal 
bodies the chains are as a rule short, usually only two indi- 
viduals (diplococci) or from three to five individuals. In 
body fluids, as milk or pleuritic exudate, however, the chains 
may reach a considerable length, 100 individuals or more. 
Upon cultivation, especially in fluid culture media, as 
bouillon, the chains are usually very long. With the diplo- 
cocci and the short chains the individuals are arranged 
longitudinally like eggs with the points against each other. 
In the longer chains the individuals are usually arranged 
transversely as eggs with their long sides against each other. 
The explanation of this condition is that in the latter ease 



40 MASTITIS OF THE COW 

the division is so rapid that the full length is never reached 
and thus through dividing the breadth of the cell is gi-eater 
than its length. 

In animal bodies the organism frequently presents a 
wide capsule. The capsule appears to occur principally on 
the short chains, especially the diplococci type. 

The capsule formation is most distinct in mice (in the 
liquid of the spleen) . In the other laboratory animals and 
in our domesticated animals it is indistinct as a rule. In 
man it is very distinct (diplococcus pneumoniae). It is 
visible after staining with carbol-methylene blue or with 
Gram's method (Fig. 6). 




Fig. 6. — The pathogenic streptococci in milk sediment. Gram. (150). Three different types. 

The streptococcus is easily stained with the common 
anilin dyes as well as bj^ Gram's method, in which decolor- 
ization with alcohol need not be long, however. It is less 
Gram positive than the staphylococcus, but more so than 
the bacillus pyogenes. The streptococcus is immotile. 

Cultivation. — It grows best at body temperature (ca. 
38° C.) and appears not to grow under 18° C. 

It grows aerobically and anaerobically but inclines more 
toward the anaerobic tendency. 

In order to isolate streptococci in pure culture, it is 
usually necessary that the culture medium contain serum. 
If one has first cultivated it on this medium it is easier to 
grow it on media without serum. 

For the purpose of isolation I pour plates of serum- 




UDDER-STREPTOMYCOSIS 41 

gelatin-agar (gelatin 5 per cent., agar 0.75 per cent., and 
serum 15 per cent., the latter is added shortly before pour- 
ing) . This medium is very soft and the colonies maintain a 
characteristic form. After one day at 38° C. the colonies 
nianifest small, grayish-white visible points, and after a 
few days a few sparse colonies in the last plate reach the 
size of ca. half a pinhead. These dis- 
tinct colonies are deep colonies. Under 
the microscope they are round or oval 
and as a rule have an uneven, jagged Vig. 7— colonies of 
or finely fringed margin which is infre- KmStin^tg^rSw: 

.1 /T7<- ^\ rrtU 1 • T. 38° C. 3 days. (X30). 

quently even [rig. 7 ) . i he colonies 
which reach the surface show a round, bluish-gray, thin, 
barely visible membranous surface growth the size of a 
hemp seed. These surface colonies are sparsely present 
and may be absent altogether. 

With stab cultures in gelatin-agar, agar (38°) and 
gelatin (20°), a grayish-white gi'anular filament forms 
along the line of puncture and as a rule there is no distinct 
sm-face growth (Fig. 8). The gelatin is 
not liquefied. Growth at 20° C. is slow. 

With streaks upon agar, coagulated 
serum (38°) and gelatin (20°) small, fine 
grayish-blue colonies like drops of moisture 
form along the streak and then coalesce, pro- 



V^ 



F,o. 8. -Culture duclug a fiuc thiu filamcut. 



of streptococci. 

geiadnigVxTs' Upon potato (38°) the streptococcus 
3 days. grows slowly without forming colonies that 

are visible to the naked eye. 

In bouillon the streptococci form grayish-white bac- 
terial granules or colonies the size of a pinhead on the bot- 
tom and along the side of the test tube. The media does 
not become turbid. Upon shaking the test tube the colo- 
nies are destroyed and the bouillon is made uniformly 
turbid. 



42 MASTITIS OF THE COW 

In milk bacteria grow without changing the medium." 

In sugar media (glucose, maltose, lactose, saccharose) 
no gas but a slight quantity of acid is formed so that the 
media can contain 1-2 per cent, normal acid. 

Resistancy. — Streptococci are verj'- sensitive. Usually 
daylight will destroy a culture in a day. In stab cultures 
or in blood in hermetically sealed capillary pipettes, kept 
from the light, the organism may hve for 3-4 months. 
Highly virulent streptococci appear to be more sensitive 
and less vigorous than those of less virulence. 

Pathogenicity. — The virulence fluctuates greatly. 
There are pathogenic streptococci which produce no lesions 
in experimental animals, others which induce local lesions 
only, and still others which cause death in variable lengths 
of time. The virulence can be raised by passage through 
animals.^ 

Mice are the most susceptible to the infection. One 
drop of bouillon culture subcutaneously can kill a mouse 
in from 1 to 7 days or sometimes longer, 14 to 21 days, 
depending upon the virulence. 

Autopsy. — If death occurs suddenly one perceives a 
slight spleen swelling, and the point of inoculation is either 

^ As a rule, the literature states that the pathogenic strepto- 
cocci coagulate milk quickly. This is insistently stated, especially 
with reference to mastitic streptococci. Of nine different strains 
of streptococci which I studied in this respect, of which seven were 
mastitic streptococci, only one strain coagulated milk. This strain 
was isolated in summer from a one-day-old milk sample; I had 
undoubtedly isolated the lactic acid streptococcus instead of a 
pathogenic streptococcus. 

The mistake in the literature mentioned probably rests upon 
this fact, since the lactic acid streptococcus is a very common 
saprophyte. 

^ The literature states that mastitic streptococci are never 
pathogenic for small experimental animals, which is often, but not 
always, the case. 



UDDER-STREPTOMYCOSIS 43 

unaltered or shows an oedematous swelling. If it runs a 
longer course the spleen is very large, and the liver may 
show small multiple areas of necrosis or abscesses and the 
point of inoculation, local necrosis with abscess formation. 

The animals usually die of bactersemia, although they 
may also die of septic intoxication without bacteraemia. 

In bactersemia the number of streptococci is small but 
tliey are comparatively numerous in the spleen pulp. 

Dogs. — These animals are also quite susceptible to the 
infection. One c.c. of a bouillon culture injected subcu- 
taneously can kill the animal in one to five days, depending 
upon the virulence. 

Autopsy. — If death occurs very suddenly the cadaver 
shows spleen swelling, serous extravasation into the ab- 
dominal and thoracic cavities and into the pericardial sac, 
lung oedema and a local oedematous swelling at the point 
of inoculation. If the course be more protracted we may 
find a serofibrinous peritonitis, pleurisy and (or) peri- 
carditis and not infrequently serofibrinous arthritis and 
pneumonia. 

As a rule the animals die of bacteraemia. Great num- 
bers of bacteria are found in the spleen pulp. If they do 
not die of bactersemia the organisms are found in great 
numbers in local nodules. 

Pigeons are somewhat resistant to the infection. They 
may be killed however in from one to two days by intra- 
muscular injection of one c.c. of a highly viiiilent culture. 

Autopsy. — A serous exudate is found in the abdom- 
inal cavity and the pericardial sac. The blood is rich in 
streptococci. 

Guinea-pigs are very resistant to the infection. One c.c. 
of a highly virulent culture injected subcutaneously in a 
guinea pig only produces local necrosis at the point of 
inoculation with abscess formation. The animal does not 
die. 



44 MASTITIS OF THE COW 

Cows. — No. 1 : Fourteen days after parturition a milch 
cow was injected in one teat with 10 c.c. of a very virulent 
bouillon culture of streptococci which had been isolated 
from a case of mastitis. The culture was controlled for 
pathogenicity on two mice, one of which died in one day, the 
other in two days. 

On the day after the infection the body temperature 
was 41.1° C. (ca. 106° F.) . The cow lay down, sweat, and 
refused to eat. The infected quarter was greatly swollen 
and painful to pressure. The skin was tight and doughy 
to the touch. The milk of the quarter was diminished in 
quantity and presented a yellowish purulent appearance. 
jNIicroscopically it was rich in streptococci. 

Two days after the infection the fever had subsided. 
The appearance of the quarter was the same. The milk 
of the quarter was still less in quantity and consisted of a 
yellowish turbid serum plus yellow fibrin clumps. Numer- 
ous streptococci were found in the fibrin. Five days after 
the infection the swelling of the quarter was greatly in- 
creased, stone hard and somewhat less sensitive. The quan- 
tity of milk from the quarter was insignificant. The milk 
was purulent and consisted of yellow turbid serum plus 
yellow clumps of fibrin which contained few streptococci. 

One month after the infection this quarter and its milk 
showed the same appearance. The animal was then 
slaughtered. 

Autopsy. — The infected quarter was firm and very 
much swollen. The incision was somewhat dry (absence 
of milk) and the cut surface was smooth, yellowish-gi-ay 
and finn. The lobuli were small and showed no milk points 
(cross sections of fresh tubuli). Upon pressure yellow 
cylinders of fibrin were expressed. In addition five necrotic 
nodules were found which were about the size of a walnut, 
rounded, sharply circumscribed, firm and surrounded by 



UDDER-STREPTOMYCOSIS 45 

pus and a thick wall of connective tissue. The walls of 
the milk-ducts were thickened. 

No. 2: Three weeks after parturition this cow was 
inoculated in one teat with 10 c.c. of a bouillon culture 
of streptococci of less virulence, which was also isolated 
from a case of mastitis and was controlled on two mice, 
only one of which died in one day. 

On the day after the infection the body temperature 
was 39.7° C. (ca. 103.5° F.). The infected quarter of the 
udder was not noticeably changed. Its milk was of normal 
appearance but gave a rich yellowish-white purulent sedi- 
ment which contained few streptococci. 

Two days after the infection the animal was free from 
fever. The quarter was not visibly altered. Its milk was 
thick, yellowish-white and gave a rich sediment of yellow- 
ish-white pus containing few streptococci. 

Three days after the infection the quarter produced 
decidedly less milk, which was yellowish-white, thick and 
clumpy. In other respects it was the same as before. 

Five days after the infection the milk of the quarter 
was yellowish-gray and flocculent, otherwise the same. 

Six days after the infection the quarter was somewhat 
firmer. It gave a small quantity of milk which was yellow- 
ish-gray, thick as pulp, puslike and contained but few 
streptococci. 

Fourteen days after the inoculation the infected quarter 
and its milk showed the same continued alteration. The 
animal was then slaughtered. 

Autopsy. — The infected quarter was not markedly 
swollen, but thick and firm. The milk was yellowish-gray, 
puslike and thick as pulp. The incision was smeared with 
the same kind of thick pus. The cut surface was even, 
yellowish-gray and firm in its lowest part. The lobuli 
showed no milk points. Upon pressure yellow-gray fibrin 
plugs were expressed. 




46 MASTITIS OF THE COW 

Udder-infection 

The streptococcus causes milk-infection and acute 
stroma-infection. The milk-infection is the most important. 

MILK-INFECTION [Parenchymatous Mastitis^ 

This is almost always primary, very seldom secondary. 
The primary milk-infection as a rule is caused by infection 
through the teat canal, seldom through the rupture of 
tubuli in fresh wounds. The secondary milk-infection is 
one following the embolic stroma, in- 
fection. It is very infrequent indeed. 
The local condition is originally con- 
fined to one quarter, as is the usual case, 
but later other quarters may become 
infected. 
Fia. 9— Typical chronio Tlic primarv infcctiou varies con- 

etreptiomycosis. Milk infec- ■■■ *' 

trs] '^x'^^sor^EpTthXl siderably in quantity and quality, 
IXlhow'JearClea; dcpcuding upon the virulence of the 
ul°\mra1obukrcoMectTv^e iufcctious orgaulsm and the condition 

tissue thickened. Tubulea r» 1 1 IJ /j_* i»j. 1 • \ 

compressed. Cells in the in- oi tlic uduer ( timc aitcr calvmg). 

tralobular connective tissue -.-rii • i ii 

and within the tubules. A Nodular nccrosis can be produced, 

moderate number of strep- i •% ■% i i • «-» 

tococci w-ere demonstrated althoUffh I haVC UCVCr SCCU dllTUSe 

in the tubules with bacterial *-> 

**^°^- necrosis in this infection. 

The quantity and quality of the inflammation varies 
with that of the primary lesion. 

Since the infectious organisms cannot liquefy the 
coagulation necrosis, the exudate often shows a decidedly 
croupous character. 

An infectious organism of low virulence which only 
produces a circumscribed inflammation in the parts around 
the base of the teats can easily induce a chronic progressive 
condition. The quantity of milk is only slightly diminished 
by this condition, which is of little importance in the be- 
ginning. It is, however, a sufficiently good culture medium 



UDDER-STREPTOMYCOSIS 47 

for the infectious organisms present. Only the number 
of cells is slightly increased, due to the low grade inflamma- 
tion. In consequence of this the organisms multiply, enter 
new tubules and lobuli, extending the inflammation and 
from here they can spread the condition further upward 
and outward (typical chronic streptomycosis ) . 

A secondary infection frequently occurs. Colon bacilli 
and staphylococci may complicate the condition. Tuber- 
culosis and pyobacillosis may also be induced, although 
pyobacillosis is the most common secondary infection. 

In these secondary infections the new infection may 
conceal the primary infection with its own individual and 
aggressive character. 

A saprophytic invasion of an original streptococcic 
infection is infrequent and only occurs in those of the high- 
est streptococcic virulence when the cell resistance has been 
lowered. 

GENERAL CONDITIONS 

Blood infection can occur and manifest itself clinically 
by multiple arthritis, which is common in the hock joint. 
Fever can be more or less severe or be absent, depending 
upon the virulence of the organism and the condition of 
the udder. It is diminished by the inflammation so that 
the animal is free from fever after a few days, as a rule. 
Fever is seldom fatal. 

In saprophytic invasion with gangrene, fever becomes 
chronic and death may occur. 

Termination. — The condition is seldom fatal. As a 
rule it runs a course of from a few days to months and 
years to recovery. The udder usually heals with diffuse 
sclerosis and parenchymatous atrophy, which conditions are 
most severe following gangrene. 

Clinical Symptoms. — ^^Ve discriminate here between 
the acute and chronic condition. 

The course of the acute condition varies from a few 



48 MASTITIS OF THE COW 

days to months. One quarter, seldom more, is affected. 
The quarter rapidly becomes greatly swollen, hard and 
painful following a severe primary lesion, or soft, flabby 
and somewhat collapsed following a less severe primary 
lesion. 

The quantity of the milk is greatly diminished, and the 
milk is thick, yellow, puslike and often contains viscid flakes 
of fibrin. In gangrene the milk is homogeneous and 
stinking. 

Upon microscopic examination of the sediment one 
finds very few Gram positive cocci of oval shape and ar- 
ranged as diplococci or perhaps in short chains. 

In the first few days and also later the animal may 
show fever if gangrene has set in. 

The course of the chronic condition extends from sev- 
eral months to a year. 

From a clinical point of view this chronic streptomycosis 
can be divided into an atypical clu'onic and a typical chronic 
streptomycosis. 

ATYPICAL CHRONIC STREPTOMYCOSIS 

This begins suddenly as an acute inflammation, 
although the inflammation is not, or at least not completely, 
high grade but becomes chronic. 

One or more quarters are affected. The quarter is 
usually moderately swollen and very firm. Not infre- 
quently one feels hard necrotic nodules in the quarter. The 
milk is more extensively purulent and consists of a turbid 
yellow fluid plus viscid fibrin flakes, or on the other hand, 
it may present a comparatively normal appearance, but 
is diminished in quantity and contains a more or less great 
number of fibrin flakes. 

Upon microscopic examination of the sediment one 
usually finds a few oval or lancet-shaped Oram positive 
streptococci arranged as diplococci or in short chains. 



UDDER-STREPTOMYCOSIS 49 

Fever occurs in the early stages but later subsides unless 
gangrene sets in, in which case the fever becomes chronic. 

This begins imperceptibly and proceeds insidiously. 
The alteration of the udder and the milk takes place by 
slow degrees. 

One or more quarters become involved. The quarter 
is not enlarged, but often diminished in size and after milk- 
ing does not collapse at all or only slightly reduces. That 
portion of the udder around the base of the teats, especially 
the parts anterior to the teats of the fore quarters and pos- 
terior to the teats of the hind quarters, appear, after milk- 
ing, to continue to be filled with milk and to be hard to the 
touch or sclerotic. 

These pathologically altered parts increase in area by 
extending forward, backward and slowly upward. 

The quantity of milk decreases by slow degi'ees. The 
milk is at fii-st imperceptibly but later always distinctly 
changed. It coagulates on boiling because of the albumin 
contained. It is thicker, almost like cream, due to the in- 
creased number of cells, and can contain blood at the same 
time. Finally it becomes decidedly puslike and consists 
almost entirely of cells. 

Upon microscopical examination of the sediment one 
finds a great number of Gram positive streptococci in long 
chains. The condition does not present the symptom fever. 

Prognosis. — The condition is seldom fatal. High 
fever, especially when gangrene is a complication, is very 
dangerous. 

The infection certainly diminishes the functional ca- 
pacity of the diseased quarter more or less. 

Following an acute infection of short duration, how- 
ever, the functional capacity completely returns to normal, 
due to the insignificance of sclerosis. 

The chronic infection tends toward complete destruc- 
tion of function. The parenchyma of the quarter under- 



50 IVIASTITIS OF THE COW 

goes severe atrophy following pressure of the interstitial 
connective tissue, which undergoes a high grade of pro- 
liferation with induration or sclerosis of the part. 

Treatment. — Prophylaxis. — The danger of infection 
in these cases is a very great one. Udder-streptomycosis, 
especially the acute type, can pass through a cow stable 
like a high-grade enzootic disease. Therefore, isolate the 
diseased cow from the others and milk her last, and of the 
quarters of the udder, milk the diseased one last of all. Do 
not draw the infected milk upon the floor, but into a recep- 
tacle of disinfectant with the idea of preventing the further 
spread of the infection. 

The treatment proper is divided into treatment of the 
general condition and treatment of the local condition. 

Treatment of the General Condition. — Fever is treated 
with febrifuges. Camphor, five grains daily, is especially 
recommended, because it is excreted with the milk and can 
thus bring about local disinfection. If the milk of the other 
quarters is to be used, some other febrifuge must be em- 
ployed, such as antifebrin (acetanilid), which does not 
impart its taste to the milk. 

If the impaction secondary to fever is severe a purgative 
of Glauber's salts is given. 

Treatment of Local Condition. — One should milk out 
the infected quarter carefully. Then inject from 300 to 
500 c.c. of lukewarm, previously boiled 4 per cent, solu- 
tion of boric acid, which exerts a deleterious effect upon 
the growth of the bacteria without too much irritation to 
the udder tissue. This solution can remain in the udder 
without danger and can be milked out in about four hours 
(Bigoteau). 

Externally one can use a mild skin irritant, as concen- 
trated iodine solution, rubbed on daily for a day or two. 
This stimulates an acute counter inflammation and 
resorption. 



UDDER-STREPTOMYCOSIS 51 

The udder should be milked carefully twice a day, but 
not more frequently, as the udder should rest. 

If the condition is obstinate and threatens to become 
chronic one can cause the milk secretion to diminish by 
inflation with air and thus inhibit the growth of the bacteria. 
One can also combine the boric acid injection with air- 
inflation. If this does not help there is nothing left but 
to cause the udder to go dry. When it is possible, only 
the diseased quarter is induced to enter the non-lactating 
state. 

In cases of severe fever following gangrene one can 
prepare an easy path into the gangrenous mass by cutting 
ofl" the teat,^ then induce healing and sclerosis by deep 
point-firing or deep cautery into the quarter. 

In nodular necrosis the course can be shortened by oper- 
ative removal of the nodules (sequesters). 

STROMA-INFECTION 

This is somewhat infrequent and of less interest. 

The wound-infection is a complication of udder wounds. 
It presents local necrosis with subsequent suppuration and 
proceeds with or without fever. 

Secondary infection with staphylococci and colon bacilli 
are common and gangrene may also be produced. 

Wound-infections are treated following the usual sur- 
gical methods. 

Therefore one provides free drainage for the wound 
secretion, which condition diminishes the nutrient fluid 

* This treatment is somewhat dangerous, however, if the dis- 
eased cow be permitted to remain with the other cows, since after 
the operation the quarter is continuously discharging infected 
milk, which spreads the infectious organisms and may be a source 
of infection to the healthy cows. Therefore the diseased animal 
must be well isolated after the operation and her stall must fre- 
quently be disinfected. 



52 MASTITIS OF THE COW 

media for the bacteria. Necrotic parts are removed early 
as a prophylaxis against gangrene. The wounds are 
cleansed once or twice a day with a mild antiseptic. 

As the development of inflanmiation is delayed by 
severe primary lesions, so wounds may be treated by in- 
flammatory irritants, as iodine solution, or with cautery. 
Both of these methods are of a disinfecting character. 

In fever febrifuges are indicated. 

An embolic stroma-infection may perhaps occur. It 
is undoubtedly rare, however. 

The primary condition inducing the blood infection is 
probably in this case a streptococcic endocarditis, at least 
such is the case in most instances. In one case of infectious 
endocarditis that I observed the cow showed evidences of 
streptomycosis. Streptococcic endocarditis appears to be 
quite rare, however. 

Following penetration of the necrotic tubuli by the 
primary lesion, i.e., by the embolic nodule, or following 
ulceration of the tubule, a secondary infection is induced. 

It probably appears clinically as a suddenly occurring 
milk-infection ( parenchjnnatous mastitis) affecting one 
or more quarters but usually one or both hind quarters. 

Summary 

I. Infectious organism: the pathogenic streptococcus. 
Character. 
Occurrence. 
Morphology. 
Cultivation. 
Resistance. 
Pathogenicity. 
II. Udder-Infection. Udder-streptomycosis. 

A. Milk-infection [parenchymatous mastitis]. 
Local conditions. 
General conditions. 
Termination, 



UDDER-STREPTOMYCOSIS 53 

Clinical symptoms. 
Acute streptomycosis. 
Chronic streptomycosis. 
Atypical chronic streptomycosis. 
Typical chronic streptomycosis. 
Prognosis. 
Treatment. 
B. Stroma infection [interstitial mastitis]. 
Wound-infection. 
Embolic stroma-infection. 



CHAPTER VII 
UDDER-STAPHYLOMYCOSIS 

The Infectious Organism 

The infectious organism is the pathogenic staphylococ- 
cus pyogenes. 

The species name pyogenes which means pus producing 
is becoming obsolete since the pathogenic staphylococcus 
can cause necrosis without suppuration. 

Characteristics. — The pathogenic staphylococcus is a 
small round microorganism which appears alone or in 
groups of two or more, or presents square or iiTegularly 
formed groups of individuals. They are easily stained 
with the common anilin dyes and after Gram's method. 
Their growth on culture media is vigorous, especially the 
surface growths. It liquefies gelatin and coagulates milk. 

Occurrence. — This coccus is similar to the streptococ- 
cus in its geographical distribution and is present every- 
where in Sweden. It is very common and appears fre- 
quently in the dust of cow stables. 

Morphology. — The size of the pathogenic staphylococ- 
cus is somewhat variable. There are large and small cocci. 
As a rule it is one micron in diameter and somewhat 
regularly globular in shape. It frequently occurs as a 
single coccus or monococcus and also joined in groups. 
These groups consist of two (diplococci) or more indi- 
viduals, such as a four-sided group consisting of from four 
to six individuals, or as an irregularh^ shaped group simu- 
lating the arrangement of a bunch of grapes. These 
groups consist of from 20 to 100 or more individuals. 

Not infrequently these cocci may also be arranged in a 
line forming a chain, which is, however, short. The mono- 
and diplococci occur in the gi'catest numbers, while the 

54 



UDDER-STAPHYLOMYCOSIS 55 

groups are less frequent and may be absent altogether 
(Fig. 10). 

As previously stated, they are easily stained with the 
common anilin dyes and following the method of Gram. 
They are immotile and do not form a capsule. 

Cultivation. — The staphylococcus grows best at body 
temperature (ca. 38° C. ) . It also grows well at room tem- 
perature. It grows aerobically and anaerobically, but 
somewhat better aerobically, however. It can be cultivated 
on the common media and grows well without serum. 

In the serum-gelatin-agar plates colony formation is 
distinct after one day at 38° C. After two days the deep 




« 




Fig. 10. — Pathogenic 

staphylococci in croupous Fig. 11. — Colonies of staphylococci, a. Deep 

membrane from udder. colonies. 6. Superficial colonies. Serum-gelatin- 

Gram. (X550). agar plates. T. 38° C, 2 days (30). 

colonies in the last plate appear as sparse pinhead size 
whitish-yellow, round or oval points. 

Upon microscopic examination with 30 diameters en- 
largement they are opaque (black) , coarsely granular and 
in consequence of this granularity show a crenated margin. 
Surface colonies are numerous and form porcelain-white 
or yellow circular or at times irregularly formed, elevated 
knob-shaped growths ca. 6 mm. in diameter (Fig. 11). 

The staphylococcus frequently produces a yellow pig- 
ment by which the colonies, especially the surface colonies, 
become a distinct yellow color. We differentiate the white 
and yellow staphylococcus. The white staphylococcus 
occurs more frequently than the yellow in our domesticated 
animals. 



56 MASTITIS OF THE COW 

In stab cultures in gelatin-agar and agar at 38° C. it 
forms a nail-like growth (Fig. 12). The nail-like growth 
in the stab is wedge-shaped and most vigorous near the 
top. The head of the nail or surface growth is thick and 
glistening and covers the greater part of the surface. In 
gelatin stab culture at 20° C. the growth is similar, the 
medium is liquefied more or less quickly (ca. 3 days) in 
goblet or funnel shape (Fig. 13) . The liquefied medium is 
diffusely turbid and has a dense bacterial deposit on the 
floor against the unliquefied medium, but at the expense of 
the surface growth. 

In streak cultures upon agar, potato and coagulated 
Fig. 12. Fig. 13. blood scrum at 38° C. they form elevated 
beaded round colonies which coalesce and 
produce a thick band along the streak. 

In bouillon the organism grows with dif- 
fuse turbidity of the medimn and forms 
\j dense bacterial deposits on the bottom of the 
F^. 12.— Culture of tubc. It docs uot prcscut a surface growth. 
BMum^-gdati^iagar t! Milk at 38° C. is usually somewhat 
Fia!' 13.— Culture of slowlv coaffulated, a condition which en- 

staphylococci. btab in . o ' 

10 days. Horif-Bhap^d ^^^^^ foF from scvcral days to a week, 
liquefaction. usualty thrcc to five days. 

In media which contain sugar, i.e., glucose, maltose, lac- 
tose, and saccharose, it forms acid but no gas, so that the 
medium finally contains ca. 2 per cent, normal acid. 

Resistancy. — The staphylococcus does not form 
spores, although it is very resistant. It resists light and 
drying in a sealed culture tube for a year or probably 
longer. It endures daylight very well. 

Pathogenicity.— The virulence varies greatly. There 
are pathogenic staphylococci which produce no alterations 
when injected subcutaneously, others which only cause local 
necrosis and abscess formation and again others which cause 
death rather quickly. 



U 

Fig. 
staphylococci. Stab in 



UDDER-STAPHYLOMYCOSIS 57 

I have not seen bacteremia in laboratory animals, al- 
though it may be produced in dogs. At the point of inocu- 
lation, however, the organism can be found. 

Autopsy of cases which have run an acute course shows 
only an oedematous swelling at the point of inoculation 
and no distinct lesions elsewhere. 

Mice, dogs and pigeons may be killed in one day by an 
organism of high virulence. 

Cows. — Twelve c.c. of a one-day-old culture of staphy- 
lococci which had previously been isolated from a severe 
case of mastitis was injected into one teat of a milch cow 
about six months after parturition. This staphylococcus 
had been preserved in culture for sixteen months sealed 
with paraffin and kept from the light. An abscess was 
produced at the point of inoculation in a control mouse. 

Before inoculation the quarter of the udder showed no 
alterations. The milk was of normal appearance but less 
in quantity and showed a yellow sediment consisting of 
a few pus cells and streptococci. 

Four hours after inoculation the body temperature was 
39.1° C. [102.2° F.]. 

On the day following the infection the animal was 
free from fever. The quarter was moderately swollen and 
was more firm to the touch than usual, but not painful. 
The quantity of milk was reduced and the milk yellow 
and thick and contained a copious sediment composed of 
yellow pus, staphylococci in great numbers and some strep- 
tococci. 

Two days after the inoculation the milk was yellow 
and thick and contained a moderate amount of sediment 
consisting of yellow pus and frequent chains of cocci. It 
was otherwise the same. 

Three days following infection the milk was whitish- 
gray and flocculent and presented a moderate quantity of 
sediment consisting of yellow, fibrinous pus and a moderate 



58 MASTITIS OF THE COW 

number of chains of cocci. Other changes were the same 
as above described. 

Four days after the infection the consistency of the 
quarter was the same as before inoculation. The milk 
showed a normal appearance again and a lessened quan- 
tity of sediment, which consisted of pus and a moderate 
number of chains of cocci. 

Six days after infection this condition remained un- 
changed. Upon cultivation of the sediment of the milk 
on serum-gelatin-agar plates a moderate number of strep- 
tococci but no staphylococci were found. 

Thirteen days after the inoculation the condition re- 
mained unchanged and the animal was slaughtered. 

Autopsy. — The infected quarter was slightly swollen 
and firm. The incision was juicy with milk. The lower 
part of the cut surface was even and uniform, grayish- white 
and yellow. The lobuli here present no milk points. Upon 
pressure here and there small yellow fibrin cylinders were 
expressed ( chronic streptomycosis ) . 

The virulence of the staphylococcus was obviously not 
high and the infection did no more to favor drying of the 
quarter than did the subsequent streptococcic sclerosis. 
Therefore I only obtained a mild infection of the udder 
which reached its height as a catarrhal inflammation in 
four days. The chronic streptococcic infection was obvi- 
ously favored b^?^ this short secondary infection. 

Udder-infection 

The pathogenic staphylococcus causes milk-infection 
and acute stroma-infection. The milk-infection is the most 
important. 

MILK-INFECTION [Parenchymatous Mastitis^ 
This is always primary and as a rule is caused by 
infection through the teat canal, seldom by infection through 
fresh wounds. 



UDDER-STAPHYLOMYCOSIS 59 

The local condition as a rule is confined to one quarter 
but may, however, be extended to more quarters, especially 
by highly virulent organisms. 

• The primary lesion varies with the virulence of the 
organism and the condition of the udder. Shortly after 
parturition, especially, a primary lesion can develop into 
diffuse necrosis of the infected quarter. 

In this manner the infection manifests its relation with 
Nocard's staphylomycosis of sheep: " Mammite gangre- 
neuse de la brebis." 

The quantity and quality of the inflammation varies 
with the primary lesion. The infection appears to have 
no tendency toward chronicity. 

Secondary infection may occur in the form of strep- 
tomycosis, colibacillosis, pyobacillosis and tuberculosis. 

These secondary infections are marked as a rule by the 
predominant staphylococci. Later, where the staphylococ- 
cus has completely run its course, the condition can be 
continued as a chronic infection as streptomycosis, pyoba- 
cillosis, or tuberculosis. 

A saprophytic invasion is common following a severe 
primary lesion, but otherwise infrequent. 

The General Condition. — Infection of the blood ap- 
pears to occur very infrequently. 

The intoxication varies with the virulence of the or- 
ganism and the condition of the udder, i.e., with the quality 
and quantity of the primary lesion. 

The fatal septic intoxication may easily follow diffuse 
necrosis of the infected quarter, especially if gangrene 
develops. 

Termination. — The condition may be fatal. The 
course is always acute and varies from a few days to three 
weeks. If the infection is removed by the inflammation 
the condition usually develops into a low-grade sclerosis. 

Clinical Symptoms. — The condition is always acute. 



60 MASTITIS OF THE COW 

as previousl}' stated. The quarter is more or less severely 
swollen and hard. The quantity of milk is more or less 
diminished. The milk may contain a red-colored serous 
fluid, indicating a primary lesion of diffuse necrosis, or 
consist of a yellow, thick, purulent fluid indicative of in- 
flanmiation and which may contain free yellow croupous 
membranes in severe udder conditions. 

Upon microscopical examination of the sediment one 
obsem^es Gram positive staphylococci as mono- or diplococci 
but seldom in groups. 

When the primar}^ lesion is severe the condition is ac- 
companied by fever, which is \'ery high if gangrene sets in. 
When the inflammation begins fever disappears. 

Prognosis. — In recently fresh and good milking cows 
the prognosis is less favorable. A severe primary lesion 
without indications of inflammation (emigration of leuco- 
cytes ) , but with high fever, is a veiy unfavorable symptom 
and is indicative of a fatal termination. Gangi-ene is also 
a very unfavorable sign. 

Inflammation with purulent milk and reduction of 
fever is a very good indication. 

Treatment. — Prophylaocis. — The condition may be 
entirely infectious. Therefore one should observe the com- 
mon measures for prevention of infection. One should 
be particularly careful to see that cows which have recently 
freshened do not come in direct or indirect contact with 
the patients through the milking process. 

The actual treatment is principally the same for udder- 
streptomycosis. 

In cases which present a severe primary lesion without 
inflammation but with high fever one may endeavor to 
save the life of the animal by extirpation of that half of the 
udder which contains the diseased quarter. 

If one does not favor this operation he may apply deep 
cautery or deep point-firing into the quarter. 



UDDER-STAPHYLOMYCOSIS 61 

Amputation of the teat before gangrene has set in is 
not to be recommended, since saprophytic invasion is thus 
made easier and this dangerous complication encouraged. 

In abscess formation one may shorten the course of 
the affection by incising the abscesses which are accessible 
for the operation. 

STROMA-iNFECTiON [Interstitial Mastitis^ 

The stroma-infection only occurs as a wound-infection 
and is therefore a complication of an udder wound. 

It is a comparatively harmless condition as long as it 
does not become complicated with a milk-infection. 

Septic-intoxication does not take place so readily be- 
cause of the lack of nutrient media for the bacteria. 

It progresses to localized wound necrosis with suppura- 
tion. Secondary infection with streptomycosis and coliba- 
cillosis is not uncommon, and gangrene may also develop. 

This wound-infection is treated following the common 
surgical methods. 

Summary 

I. Infectious organism: the pathogenic staphylococcus. 
Characteristics. 
Occurrence. 
Morphology. 
Cultivation. 
Resistancy. 
Pathogenicity. 
II. Udder-infection, Udder-staphylomycosis. 

A. Milk-infection [parenchymatous mastitis]. 
Local conditions. 

General conditions. 
Termination. 
Clinical symptoms. 
Prognosis. 
Treatment. 

B. Stroma-infection [interstitial mastitis]. 
Wound-infection. 



CHAPTER VIII 

UDDER COLIBACILLOSIS 

Infectious Organism 

The infectious organism is the colon bacillus or bacillus 
coli. The name coli is taken from its original habitat, the 
contents of the colon of man. 

The mastitis bacillus described by Kitt as the bacillus 
phlegmasi^e uberis may be briefly reviewed as the colon 
bacillus. Kitt's bacillus should have only one flagellum 
while the genuine colon bacillus should have from four 
to six flagella. We have so little practical knowledge 
concerning the flagella of the bacilli that we should venture 
to distinguish new types only upon the difference in their 
number. 

Characteristics. — The colon bacillus is a short thick 
rod with rounded ends. It is easily stained with the com- 
mon anilin dyes, but is not stained after Gram's method. 
The growth in the common culture media is vigorous, 
especially surface growths. It does not liquefy gelatin. 
It coagulates milk with gas production. It splits sugars, 
as glucose, maltose, lactose, and also often saccharose with 
the production of gas and acid. 

Occurrence. — The colon bacillus, as is the case with 
the other organisms, is of uniform geographical distri- 
bution and occurs everywhere in Sweden. It is a common 
intestinal parasite and therefore occurs in manure and in 
the dirt and dust of cow stables. 

Morphology. — The size of the colon bacillus varies 
considerably. There are large and small colon bacilli. The 
longer vary between one and four microns; only in excep- 
tional cases it is longer, at which times it may reach eight 
microns. Its thickness varies between 0.5 to 1.5 microns. 

G2 







UDDER-COLIBACILLOSIS 63 

As a rule the size of the bacillus is regularly two to three 
microns long. 

The vegetative colon bacillus forms a distinct but, in 
comparison with its thickness, somewhat short rod with 
rounded ends. It seldom reaches the unusual length of 
eight microns, at which times it simulates a short thread. 
Besides these vegetative specimens one always finds a num- 
ber of shorter specimens which have an oval form and many 
of which are also globular. The short forms are most numer- 
ous in culture; they are less numerous in the animal body 
where the vegetative speci- 
mens are present in the 
greatest number. 

The colon bacillus oc- 
curs mostly as a single ba- 
cillus, but is also arranged 

in lines consisting of two Fig. 14— ColonbacUliinmilk sediment. Carbol- 
.~- . „-. methylene blue. ( X 150.) Two different cases. 

mdividuals or diplobacilli, 

infrequently of three individuals or streptobacilh (Fig. 14) . 

They are easily stained by the common anilin dyes, 
but are quickly and easily decolorized following Gram's 
method. 

In preparations from animal bodies it is surrounded 
by a bright halo like a capsule. This is perhaps an effect 
produced by the flagella. 

The colon bacillus is motile or immotile.^ 

Cultivation. — It grows best at body temperature 
( 38 ° C. ) , it also grows well at room temperature. It grows 

^ I classify the immotile bacterium lactis aerogenes (synonym: 
b. acidi lactici) with the colon bacillus. The real colon bacillus is 
motile, b. lactis aerogenes is immotile ; but in other morphological 
and cultural characteristics these bacteria are very similar. The 
real colon bacillus often forms " wander zones " in culture, which 
formations are not produced by b. aerogenes. Both of these bac- 
teria produce mastitis. 



64 



MASTITIS OF THE COW 



aerobically and anaerobically, but better aerobically. It also 
grows well on the common culture media without serum. 

In serum-gelatin-agar plates at 38' C. the growth is 
distinct after one day. After two days sparse deep colonies 
form in the last plate which are the size of a pinhead, 




Fia. Ic 



-Deep colonies of colon bacilli with and without daughter colonies, 
agar plates. T. 38° C, 2 days (X 30;. 



yerum-gelatin- 



yellowish-white, round points which are not infrequently 
surrounded by one or more broad, grayish-white zones. 
This zone is produced in the cultui'e media by the bacilli 
which wander out from the colony. The zone can therefore 
be called the " wander zone." 

Under the microscope the colonies are almost trans- 
parent, yellow, romid or rounded and have 
an even or coarsely crenated margin. 

The colonies with "wander zones" show 
a large colony in the middle, the mother 
colony, which is surrounded by a more or 
less broad ring of peripheral or daughter 
colonies. These colonies present growing 
margins depending upon the outwandering 
of bacilli (Fig. 15). 
The surface colonies are numerous and form bright gray 
round or irregularly lobed thin coverings from 6 to 10 mm. 
Under the microscope they often show a granular centre 
which depends upon the formation of tlie colonies in the 
media (Fig. 16). In stab cultures in gelatin-agar (Fig. 
17) , agar at 38° C, and gelatin at 20° C. the colonies form 




Fia. 16. — Surface 
oolony of colon bacilli. 
Serum - gelatin - agar 
plates. T. 38° C, 2 
days (X 10). 



UDDER-COLIBACILLOSIS 



65 



a nail culture. The nail is wedge-shaped, most vigorous 
above and often has a fine felt-like contour following the 
formation of daughter colonies in the media by outwander- 
ing bacilli (Fig. 18). In soft media like gelatin- agar the 
nail-like growth is often surrounded by a whitish-gray 
more or less thick cylindrical zone (wander zone), and the 
nail-shaped growth in the track of the stab, the stab growth, 
can become indistinct by a vigorous outwandering of bacilli. 
The nail head is made of a grayish-white somewhat thin 
surface membrane which at 38° C. completely covers the 
surface and in gelatin at 20° C. is small and only covers 
part of the surface. Gelatin is 
not liquefied. 

In streaks upon agar at 38° C. 
it forms whitish-gray round colo- 
nies, which coalesce and produce a 
gray band along the streak. In 
bouillon and peptone water at 



Fig. 17. 



Flo. 18. 



\J 



1! 



Flo. 17. — Cultures of colon bacilli. 



3 days. Two different strains, a. with- 
out and b. with "wander zone." 

Fio. 18. — Culture of colon bacilli. 
Stab in gelatin. T. 20° C, 6 days. 
With downy hair-like peripheral 
outgrowth. 



38° C. the colon bacillus grows ^*ll^.i"^^^:^.^-it'i'i""A^'!!::„J-.^!°:5i' 
with diffuse turbidity of the cul- 
ture media and formation of 
distinct bacterial deposits on the 
bottom of the test tube. As a rule it does not form a 
membrane on the surface, and if it does it is very thin and 
small. 

The colon bacillus coagulates milk somewhat quickly, 
usually in one day, at 38° C, with the production of gas. 

It splits the sugar, glucose, maltose, lactose, and often 
saccharose with formation of gas and acid so that the 
medium finally contains 2 to 3 per cent, normal acid. The 
splitting of saccharose is slow and does not occur at all with 
some colon bacilli. 

The colon bacillus produces more or less indol in pep- 
tone water (peptone Witte 3 per cent., sodium chloride 
0.5 per cent.) in about six days at 38° C. 

5 



66 MASTITIS OF THE COW 

The colon cultures have a strong, unpleasant, burnt 
odor. 

Resistancy. — The colon bacillus does not fonii spores 
but is nevertheless very resistant. It can live a year in a 
culture kept in the dark and sealed to prevent drying. 

Pathogenicity. — The vii-ulence is very variable. In 
subcutaneous inoculations of laboratory animals certain 
colon bacilli manifest no alterations. Others produce only 
a local necrosis with abscess formation, while others may 
kill the animal more or less quickly. 

As a rule, laboratory animals die of bacter^emia. 

On autopsy one finds a more or less enlarged spleen, 
and the point of inoculation in the subcutis is oedematously 
swollen or manifests necrosis with inflammation in the sur- 
rounding tissue. There are no other distinct lesions. 

Mice are very susceptible to the infection. They may 
die in from one to twelve days. As a rule they die in about 
three days, seldom after a course of a week or more. 

A dog inoculated subcutaneously with a virulent culture 
did not die but showed a necrotic nodule at the point of 
inoculation. 

A guinea-pig was inoculated subcutaneously with a 
virulent culture and showed a widespread severe oedema- 
tous swelling at the point of injection and also bacter^emia. 

A pigeon inoculated in the pectoral muscle with a viru- 
lent culture did not die but developed a necrotic nodule at 
the point of injection. 

Cows. — About six months after calving a cow was in- 
jected in one teat with 10 c.c. of a one-day-old bouillon 
culture of colon bacillus which had previously been isolated 
from a case of mastitis. Of the two control mice one died 
in two and the other in three days. 

Examination of the quarter before infection showed no 
alterations. The milk was of normal appearance but con- 
tained a small quantity of sediment consisting of yellow 
pus which contained a few streptococci. 



UDDER-COLIBACILLOSIS 67 

Five houi's after the infection the body temperature 
was 39.1° C. (102.2° F.). 

On the day after the infection the appetite was dimin- 
ished and the animal showed constipation. The infected 
quarter was swollen, firm, red, warm and painful. The 
quantity of milk was diminished. The reaction of the 
milk was alkaline. It was yellow, thick and purulent and 
presented a copious sediment of pus which contained a few 
colon bacilli. 

Two days after the infection the fever had subsided the 
milk was yellow, thick and purulent and contained a rich 
purulent sediment which showed a few colon bacilli. Other 
conditions were the same. 

Three days after the infection the swelling of the quar- 
ter had subsided. The quantity of the milk, however, re- 
mained small. The milk showed a normal appearance but 
was yellow and somewhat flocculent and contained a slight 
sediment consisting of yellow fibrinous pus containing a 
few streptococci. Upon cultivation of the sediment by 
plating a large number of streptococci but no colon bacilli 
were recovered. 

Four days after the infection the milk was decreasingly 
less. The milk was of normal appearance but contained a 
smaller quantity of sediment consisting of yellow fibrinous 
pus showing few streptococci. It was otherwise as before. 

Sixteen days after the infection this condition was un- 
changed. The animal was then slaughtered. 

Autopsy. — The infected quarter was slightly swollen 
and its consistency a little firm. The incision was moist 
with milk. The lower part of the cut surface even, smooth, 
grayish-white and firm. The lobuli showed no milk points 
here. Upon pressure yellow fibrin cylinders were expressed 
(chronic streptomycosis). 

The virulence of the colon bacillus in this case was 
somewhat great; the udder had shown a tendency to go 



68 MASTITIS OF THE COW 

dry and in consequence of the chronic streptococcic infec- 
tion presented less favorable conditions for the infection. 

Consequently, I obtained a severe udder-infection with 
fever which was quickly eliminated by a catarrhal inflam- 
mation in three days in consequence of the conditions 
already named. The chronic streptococcic infection was 
at first concealed by this secondary infection but later again 
appeared and then became more severe. 

The similarity to the experiment with staphylococci is 
apparent. 

Udder-infection 

The colon bacillus causes milk-infection and acute 
stroma-infection. These infections manifest a great simi- 
larity to those produced by staphylococci. 

MILK-INFECTION [Parenchymatous Mastitis'] 

This is the most important. It is always primary and 
is caused by infection through the teat canal, seldom 
through infection of a fresh wound. 

The local condition is usually confined to one quarter 
but can involve more quarters by infection (for example, 
during milking) . The primary lesion varies with the viru- 
lence of the infectious organism and the condition of the 
udder. A superficial or moderately deep necrosis is the 
most common. A diffuse necrosis of the udder seldom 
occurs. 

The quantity and quality of the inflammation varies 
with that of the primary lesion. The inflammation can 
be of a catarrhal or croupous nature. The infection shows 
no tendency toward chronicity. 

Secondary infections may occur with strepto- and sta- 
phylomycosis, as well as with pyobacillosis and tubercu- 
losis. 

In this case the staphylomycosis can conceal the coli- 
bacillosis while the others as a rule may become masked by 



UDDER-COLIBACILLOSIS 69 

the vigorous colibacillosis ; but later, when the colon bacillus 
is eliminated, these chronic infectious conditions, strepto- 
mycosis, pyobacillosis, and tuberculosis, may proceed. 

A saprophytic invasion of an original colibacillosis is 
infrequent. 

General Conditions. — A secondary blood infection is 
seldom produced. 

Intoxication varies with the virulence of the organism 
and the condition of the udder. Soon after calving the 
infection can cause a high-gi'ade, probably fatal, septic 
intoxication accompanied by severe symptoms of fever. 

Termination. — The simple colibacillosis is seldom 
fatal. The infection is eliminated by a more or less severe 
inflanmiation which lasts from three days to about three 
weeks. The subsequent sclerosis is usually of a low grade. 

Clinical Symptoms. — The condition is always acute. 
The infected quarter is more or less severely swollen and 
hard. At first it is painful but later not sensitive. 

The quantity of milk is diminished. The milk either 
forms a grayish- white, turbid serous fluid (primary lesion) 
or yellow, thick purulent fluid (inflammation which in 
severe primary lesions contains yellowish clumps of croup- 
ous membranes ) . 

Upon microscopic examination of the sediment. Gram 
negative colon bacilli are seen as single rods or diplobacilli. 
They are somewhat large and thick and show rounded 
ends. In the stage of the primary lesion they are some- 
what numerous, but in the stage of inflammation during 
the emigi-ation of leucocytes their number is smaller. 

The condition is accompanied with fever which may 
be very high. With the beginning of inflammation fever 
is reduced. 

Prognosis. — In these cases the prognosis is always 
good, although in cows which have recently freshened the 
prognosis is less favorable. 



70 MASTITIS OF THE COW 

Unfavorable symptoms are high fever and repressed 
leueocytic emigration, checked inflammation. 

Treatment. — The condition is treated in the same 
manner as streptomycosis (see streptomycosis). 

STROMA-iNFECTioN [Interstitial Mastitis] 

The stroma-infection occurs only as a wound infection 
which is a complication of an udder-wound. It is an ex- 
tremely harmless condition and usually presents a super- 
ficial wound necrosis with subsequent suppuration. 

Secondary infection with strepto- and staphylomycosis 
is common and gangi*ene can also occur. 

These wound infections, like the previous wound infec- 
tions, are treated following the usual surgical methods. 

Summary 

I. Infectious organism : the colon bacillus. 
Characteristics. 
Occurrence. 
Morphology. 
Cultivation. 
Resistancy. 
Pathogenicity. 
II. Udder-infection. Udder colibacillosis. 

A. Milk-infection [parenchymatous mastitis]. 

Local conditions. 
General conditions. 
Termination. 
Clinical symptoms. 
Prognosis. 
Treatment. 

B. Stroma-infection [interstitial mastitis]. 

Wound-infection. 



CHAPTER IX 

UDDER-PYOBACILLOSIS 
Infectious Organism 

The infectious organism is the pyogenes bacillus, ba- 
cillus pyogenes. 

Chaeacteristics. — The bacillus pyogenes is a very 
small thin bacillus. It stains slowly and faintly with the 
common anilin dyes but stains well after the method of 
Gram. Its growth on the usual culture media is thin, 
especially the surface growths. It liquefies coagulated 
serum and gelatin after a somewhat longer time. It coagu- 
lates milk. The organism is found in Germany, Holland, 
Denmark and Sweden. This indicates that it is of wider 
distribution, although it has not been reported since it was 
briefly studied by Grips, Glage and Nieberles. It can be 
found here and there in the various districts of Sweden. 

It appears to be present frequently in the digestive 
tract of cattle since it is often found in diseased nodules 
produced by foreign bodies in the reticulum. One may 
therefore assume that it is to be found in the dirt and dust 
of our cow stables. 

Morphology. — The bacillus pyogenes is a small and 
very fine rod. Its size varies somewhat. It is 1 to 3 microns 
long and 0.2 to 0.3 micron thick. As a rule, the bacillus 
is 2.5 microns long and 0.2 micron thick. In dimensions 
it most closely resembles the erysipelas bacillus and also 
the tubercle bacillus, except that the latter is a little larger. 

The bacillus pyogenes is usually rod-shaped. Only in 
cultures, especially on coagulated serum, does the organism 
assume an oval or nearly round shape in consequence of 
rapid multiplication. 

This organism usually appears singly in smear prepara- 

71 



72 JVIASTITIS OF THE COW 

tions. It seldom presents chains, which are short and com- 
posed of one or two, frequently three, individuals. The 
bacilli often lie parallel to each other or slightly converging 
so that groups may be formed (Fig. 19) . 

It is stained with difficulty by the common anilin dyes, 
but stains well after the method of Gram, but even here 
one must not too strongly decolorize it with alcohol. They 
are less Gram positive than the streptococci, but more 
so than the malignant oedema group. 

Cultivation. — The bacillus pyogenes grows some- 
what slowly at body temperature {3S° C.) and very slowly 
and weakly at 20° C. It does not appear to grow at room 
temperature (15° C). It grows aerobically and anaero- 

bically, but shows more of an 
anaerobic character. In order 
to isolate it a pure culture 
^^ medium containing serum is 
necessary, but after it has been 

F,o. 19.-Pyo.enes bacilli in milk sediment. iSOlatcd it CaU bc grO™ OU thC 

Gram. (X 550). commou mcdia without serum. 

In serum -gelatin-agar plates at 38° C. the growth is at 
first visible after from two to four days. The deep colonies 
in the first plate then appear as sparse small whitish-gray 
scarcely visible points the size of the hole made by a pin 
prick. 

Under the microscope the colonies appear as veiy small 
bright yellow round or rounded structureless vesicles with 
even margins. The larger colonies appear to be produced 
by the grouping of a greater or lesser number of these 
vesicles into a composite mass like a raspberry and there- 
fore present an irregular shape and a crenated margin. 
The smaller colonies are probably produced by one bac- 
terium, " primary or single colonies," and the larger ones 
by coalescence of the primary colonies, " complex colonies " 
(Fig. 20). 




UDDER-PYOBACILLOSIS 



73 




O 



O 



O 



O 



Fig. 20. — Deep colonies of pyogenes 
bacilli. Serum-gelatin-agar plates. T. 
38°, 2 days (X30). 



As a rule one searches vainly for surface colonies and 
if he finds one it is extremely thin and consists of a scarcely 
visible whitish-gray round layer about 2 mm. in diameter. 
In stab cultures in gelatin- agar and agar at 38° C. the 
bacillus pyogenes produces a growth in the line of the stab 
after two to five days which re- 
sembles a thread. Usually no 
growth occurs on the surface, but 
when present appears as a fine 
gray point over the opening in 
the stab puncture (Fig. 21 ) . In 
gelatin stab cultures the growth 
is slow and scanty. It also forms 
a thread-like growth along the 
line of puncture in the media 
which shows infundibuliform liquefaction along the stab 
after a week, following which the bacteria form a small 
deposit on the bottom made by the firm media (Fig. 22) . 
On streak cultures on coagulated serum at 38° C. it 
forms a fine scarcely visible gray thread 
along the streak in about four days. After 
six days on the media liquefaction occurs 
forming a moist glistening groove along 
the streak. 

In bouillon the bacillus gi*ows in from 
two to four days at 38° C. without turbid- 
ity of the media, but shows small fine gray 
granules which sink to the bottom of the 
tube, foi-ming a granular deposit. Upon 
shaking the tube these deposits cause the 
media to become diffusely turbid. 

The bacillus pyogenes coagulates milk at 38 



Fig. 21. 



Fig. 22. 



\J 



\J 



Fia. 21.— Stab cul- 
ture of pyogenes bacilli 
in serum-gelatin-Ggar. 
T. 38° C, 4 davs. 

Fiq. 22.— Stab cul- 
ture of pyogenes bacilli 
in gelatin. T. 20° C, 
12 days. 



»°C. intwo 
to three days and the coagulum thus formed later liquefies 



with the formation of whey. 



74 MASTITIS OF THE COW 

In dextrose media the bacillus pyogenes produces acid 
but no gas. The media can then contain 1.3 per cent, nor- 
mal acid. In maltose, lactose, and saccharose media it 
forms neither acid nor gas. 

Resistaxcy. — The bacillus pyogenes is very sensitive. 
Usually daylight can kill it in culture in a few days. It 
can be kept for two months in cultures not exposed to the 
light and sealed to preserve moisture. 

Pathogenicity. — B. pyogenes is a typical pus pro- 
ducer and induces its effect slowly. Therefore it does not 
cause an acute but a chronic infection. It causes suppura- 
tive foci at the point of inoculation. The animals never die 
of bacteremia. 

Mice manifest a subacute infection usually with no 
alterations. One mouse, however, showed a chronic sup- 
purative wound at the point of infection fourteen days after 
inoculation. 

Dogs frequently but not always present a subacute 
infection after about fourteen days and show abscesses con- 
taining thick yellow pus and numerous pyogenes bacilli. 
Upon intraperitoneal inoculation similar abscesses are pro- 
duced in the omentum and mesentery. Otherwise the 
health of the animal does not appear to be disturbed. 

Two guinea-pigs infected subcutaneously manifested 
no alterations after two months. 

Cows. — 1. About six months after calving a cow was 
injected in one teat with 12 c.c. of a three-day-old bouillon 
culture of bacillus pyogenes which had been isolated from 
a case of calf pneumonia. This bacillus had been grown 
on culture media for a period of three weeks. The dog 
used as a control developed a distinct abscess at the point 
of injection fourteen days after inoculation. 

Examination of the quarter and its milk before the in- 
fection revealed no pathological alterations. 

The day after infection the body temperature was nor- 



UDDER-PYOBACILLOSIS 75 

mal. The quarter was not changed. The quantity of milk 
was not diminished. The milk had a normal appearance 
but presented a small quantity of sediment composed of 
cells. The cells contained one single bacillus pyogenes. 

On the third day after infection the quarter was un- 
changed. The milk was unaltered. 

The same conditions obtained on the following day. 

Nine days after the infection the part near and behind 
the teat (this was a hind quarter that was infected) was 
swollen and presented a distinctly circumscribed round, 
hard, sensitive swelling the size of a hen's egg. The milk 
was not changed. 

This condition was the same on the following day. 

Seventeen days after the infection the skin of this part 
of the udder was oedematously swollen, firm and immovable 
and adhered to the swelling of the udder. The milk was 
yellow and flocculent and contained a moderate sediment 
which consisted of pus containing groups of bacillus 
pyogenes. 

Twenty-one days after the infection this condition re- 
mained the same. The animal was then slaughtered. 

Autopsy. — The infected quarter was swollen and firm 
around the base of the teat. The incision was purulent. 
The lower part of the cut surface even, gray and firm. The 
lobuli showed no milk points, but instead small pus points 
up to the size of a pinhead. Upon pressure yellow plugs 
of pus were expressed. Externally at the upper part of 
and behind the base of the teat there was a cavity the size 
of a walnut with thick connective-tissue wall and irregular 
lumpy interior. It contained a greenish-yellow, thick pus 
which showed large numbers of small fine Gram positive 
pyogenes bacilli. 

2. Three weeks after parturition another milch cow 
was injected in one teat with 10 c.c. of a mixture con- 
sisting of equal parts of bouillon culture of streptococci and 



76 MASTITIS OF THE COW 

bouillon culture of bacillus pyogenes. The streptococcus 
and also the bacillus pyogenes were isolated from a case 
of mastitis. The streptococcus killed two control mice, 
the first in one and the second in two days. The virulence 
of the bacillus pyogenes was not controlled. 

Examination of the infected quarter and its milk before 
infection revealed no pathological alterations. 

On the day after infection the body temperature was 
40.5° C. (ca. 105° F.). The quarter was severely swollen 
and painful, the quantity of milk was decreased and the 
milk was yellowish-white and thick and showed sediment 
consisting of pus which contained a great number of strep- 
tococci but no pyogenes bacilli. 

Two daj^s after the infection the body temperature was 
39.8° C. (ca. 103.5° F.). The milk was yellow and puru- 
lent and contained shreds of croupous membrane showing 
a few streptococci. It was otherwise as before. 

Three days after the infection the body temperature 
was 39.3° C. (102.5° F.). It was otherwise the same as 
before. 

Four days after the infection the body temperature 
was normal. The swelling of the quarter was somewhat 
reduced. It was otherwise the same as before. 

During the following day this condition remained the 
same. 

Six days after the infection the quarter showed firm 
nodular swellings here and there. The milk was yellowish- 
gray, purulent and contained croupous membranes which 
showed. a few streptococci and here and there in the cells 
small groups of pyogenes bacilli. 

During the following days this condition remained 
unchanged. 

Twenty days after the infection the quarter was in the 
same condition. The milk was yellow and pus-like and con- 
tained free croupous membranes showing few streptococci 



UDDER-PYOBACILLOSIS 77 

but many pyogenes bacilli which were for the most part 
within the cells. The animal was now slaughtered. 

Autopsy. — The infected quarter was moderately swol- 
len, irregular, nodular and of firm consistency. The in- 
cision was smeared with a thick yellowish-green pus. The 
cut surface was even, yellowish-gray and firm. The lobuli 
showed no milk points, but showed pus points distinctly. 
Upon pressure yellow pus cylinders were expressed. 
Externally seven suppurative foci were observed which 
ranged in size from a hazelnut to a walnut. They contained 
yellowish-green cheesy pus and were surrounded by a white 
thick, firm connective-tissue capsule. Nmnerous milk-ducts 
formed thick firm cords which on cross section presented 
yellowish-green pus centres and were surrounded by a 
white, thick, firm layer of connective tissue ( fistula forma- 
tion) . The yellowish-green pus contained a great number 
of small thin Gram positive pyogenes bacilli. 

Both of these experiments are good examples of infec- 
tion through transportation of the infectious organism 
by the leucocytes. The infected milk is quickly freed from 
the organisms by resorption, that is, in these cases the leuco- 
cytes pick up the organisms and carry them away. 

In the lymph-vessels a few of these phagocytes are 
destroyed by the living bacteria which they contain and 
these liberated organisms induce a stroma-infection which 
finally terminates as a secondary milk-infection by per- 
forative ulceration of the milk-ducts. 

Bacillus pyogenes so restrains itself that it simulates a 
saprophyte and leucocytes may pick it up and re-enter the 
vessels, where later it manifests its parasitic nature and 
then destroys these cells. It is therefore insidious in its 
action. It might be classed as a cell parasite instead of a 
fluid parasite because of this action toward cells. 

In the first experiment the action of the bacilli was 
slower and less widespread, because the alactiferous (dry) 



78 MASTITIS OF THE COW 

udder afforded less favorable conditions for development. 
In the last case the bacterial action was quicker and more 
widely distributed, partly because the udder was rich in 
fluid which afforded a better nutrient medium for the micro- 
organisms and partly because of the synchronous strepto- 
coccic milk-infection, circumstances, so to speak, which 
placed the tissue between two fires. 

Udder-infection 
Bacillus pyogenes always induces a stroma-infection 
first, and this can later develop into a secondary milk- 
infection by perforative ulceration of the milk-ducts. 
Therefore the stroma-infection is the most important, and 
milk-infection is only a result of it. 

STROMA-INFECTION [Interstitial Mastitis] 

The stroma-infection manifests a typical progressive 
character. 

Ports of Infection. — Infection may gain entrance 
through the teat canal, wounds, or through the blood 
stream. Infection by way of the blood follows pyobacil- 
losis of the lungs with penetration of a pulmonary vein by 
a necrotic focus. Pyobacillosis of the lungs is not alto- 
gether infrequent. It appears to be present in calves prin- 
cipally and may cause udder conditions in yearling heifers. 
The condition can be produced through an infected wound 
and is not uncommon. 

Infection through the teat canal is the most common, in 
my opinion, since the condition appears to be primary in 
the udder without presenting any wound of the udder. If 
the bacillus is brought to the mouth of the teat canal it can 
enter the milk in that canal and grow in it, and then be 
taken up by the leucocytes. In other cases a cow may lie 
down and the infection be introduced on a straw which may 
be forced into the teat canal. 



UDDER-PYOBACILLOSIS 79 

Local. Conditions. — The lesions produced in the udder 
occur in proportion to the number of organisms which gain 
entrance. The bacilH are taken up by the leucocytes in the 
capillary blood, in wounds, or in the milk and deposited in 
the stroma of the udder, where the leucocytes are finally 
necrotized by the parasites. In many cases perhaps the 
opposite condition takes place, that is, the bacilli are de- 
stroyed and the infection prevented. The infection can 
occur, however, by entrance of gi-eat numbers of bacteria, 
that is, many bacteria; but still more leucocytes are de- 
stroyed and the infectious organisms become superior to 
the leucocytes. 

An inflammatory zone forms around these necrotic cells 
(primary lesion) and outside of this zone of leucocytes a 
capsule of connective tissue develops. Secondary nodules 
are formed during the removal of the infectious organisms 
by the leucocytes. All of these foci gradually enlarge with 
subsequent atrophy of the tubules and finally ulceration 
into the tubules or outward through the wound, if one be 
present, or through the skin. 

Depending upon the point of entrance of the infection 
the following forms may be distinguished, i.e., ( 1 ) primary 
udder-pyobacillosis ; (a) udder-pyobacillosis through teat 
infection; (b) udder-pyobacillosis through wound-infec- 
tion. (2) Secondary or embolic udder-pyobacillosis. 

Primary udder-pyobacillosis usually occurs without 
pyobacillosis of the lungs. It may, however, be present 
along with the lung condition, in which case the latter may 
be either primary or secondary (caused by blood-infection 
induced by udder conditions) . 

Udder-pyobacillosis through teat infection usually 
affects a single quarter, but can then reach other quarters 
through infection, i.e., during milking. It starts around 
the base of the teats and then spreads further sideways and 
upward. 



80 IVIASTITIS OF THE COW 

Udder-pyobacillosis through wound-infection is distin- 
guished by its locahzation in the neighborhood of the wound 
and by a comparatively uniform distribution of the con- 
dition from this point inward. Ulceration in the wound is 
great and tends toward fistula formation. 

Secondary or embolic udder- py oh acillosis is distin- 
guished by a primary condition of the lungs and by its 
position, which usually is in several quarters in the begin- 
ning, seldom in one quarter alone. Should one quarter 
alone be affected it is most likely to be a hind quarter. It 
is further distinguished by large and somewhat uniform 
distribution in the affected quarters in the beginning. ( The 
condition is distributed in the lower parts in most instances, 
however. ) 

In the beginning these forms may be sharply separated. 
Through development of the conditions they may become 
somewhat similar. Thus, for example, primary udder-pyo- 
bacillosis through wound-infection showing secondary 
ulceration through the skin with subsequent fistula forma- 
tion can become very difficult to distinguish from the other 
forms. 

By ulceration through the milk-ducts pus containing 
infectious organisms is emptied into the milk. This pus 
can: (1) Be withdrawn with the milk without producing 
any changes in the udder ; ( 2 ) the infectious organisms can 
be picked up in the milk by fresh leucocytes and be again 
carried into the connective tissue, through which the in- 
fection is spread further, and (3) the thick pus can remain 
in the milk-ducts for a shorter or longer time, through which 
the infection, as a secondary milk-infection, can cause more 
or less necrosis of the underlying tissue and thus produce a 
croupous inflammation. Upon desquamation of this 
croupous membrane a wound is presented which likewise 
becomes infected. 

Secondary infections are common and appear to aggra- 



UDDER-PYOBACILLOSIS 81 

vate the condition greatly and to favor the primary infec- 
tion. They may be divided into milk- and stroma- 
infections. 

Secondary Milk-infection {Secondary Parenchyiriatous 
Mastitis]. — These infections may be strepto- or staphylo- 
mycosis as well as colibacillosis. The most common, how- 
ever, is the streptomycosis. They occur one at a time as a 
rule, but several secondary infections may be present at the 
same time. 

These secondary infections, especially staphylomycosis, 
may raise the condition to an acute process and thus induce 
diffuse necrosis of the quarter and cause the death of the 
animal. In the earlier stages of pyobacillosis they not 
infrequently mask the primary condition. 

In developing, pyobacillosis (with secondary milk-in- 
fection) favors the formation of croupous exudate which 
begins to form in considerable quantities in the secondary 
infection. This exudate can remain situated in a teat canal 
and in this way form a good bridge for the infectious 
organisms. 

Secondary Stroma-infection. — These secondary stroma- 
infections may be of two different kinds, acute and 
chronic. 

Acute secondary stroma-infection occurs only as a 
secondary infection to wounds. It presumes, consequently, 
a primary or a secondary wound produced by ulcer- 
ation. In these wounds secondary infection is the rule. 
These secondary infections may be strepto- or staphylo- 
mycosis or colibacillosis. They may occur one at a time 
or several secondary infections may be present together. 

The single chronic secondary infection which appears to 
occur is tuberculosis. It is infrequent. Pyobacillosis and 
its secondar}^ infection, which it somewhat resembles in 
nature, work together for the destruction of the udder. A 



82 IVIASTITIS OF THE COW 

secondary infection with actinomycosis is possible but 
occurs infrequently. 

Saprophytic invasion is common and appears to favor 
the infection. It causes milk- or (and) wound-gangrene. 

Milk-gangrene is very common. The croupous exudate 
in extensive pyobacillosis with secondary milk-infection 
predisposes toward this complication. This exudate as 
before mentioned can remain located in the teat canal and 
constitute a good bridgework. Secondary milk-infection 
also favors the beginning of this complication to a great 
extent. 

Wound-gangrene may develop in a primary or second- 
ary wound. It is very common and we may say it is the 
rule if wounds are not treated. 

General Conditions. — Blood-infection. — A necrotic 
focus may contain a vein which becomes open by perfora- 
tive ulceration and admits the bacteria which caused the 
necrosis. These organisms are carried by the venous sys- 
tem to the lungs. From the lungs the bacteria may enter 
the pulmonary veins in a similar manner and be carried 
by the arterial blood stream to one or several other organs 
of the body, inducing secondary metastatic foci. 

Intoxication. — Pyobacillosis causes a low-grade 
chronic intoxication, which, like the lesion, has a progressive 
character. It continues to a chronic progressive emaciation 
and anaemia with thickening and finally a leather}^ skin 
and roughened hair coat and finally to fever and death of 
the animal. 

Complications with acute secondary infections and 
[or] with gangrene often produce high and continuous 
fever and may terminate more or less quickly in death of the 
animal. 

Termination. — The primary condition seldom causes 
death. It advances by a chronic protracted course, extend- 
ing over months and years to progressive destruction of 



UDDER-PYOBACILLOSIS 83 

the infected quarter and not infrequently presents similar 
secondary lesions in other organs. It predisposes to the 
secondary infections and gangrene, which conditions, espe- 
cially together, terminate in death. 

In one case the infection confined itself to the cisterns 
and milk-ducts, to the exclusion of the udder which was 
nearly free from the infection. This form of the infection 
induces destruction of the mucous membrane of the milk- 
ducts with subsequent healing and connective-tissue forma- 
tion, which closes the lumen of the ducts, with the result 
that the cisterns present a white vault-like connective-tissue 
dome without any openings for the milk-ducts. In con- 
sequence of these alterations the udder shows milk stasis 
with distended lobuli and tubuli together with a firm con- 
dition due to sclerotic eonnective-tissue proliferation. 

Clinical Symptoms. — The condition is chronic. One 
or more quarters are affected. The diseased quarters are 
nodular and swollen in their lower extremities. These 
nodular foci are hard and painful or soft and then fluctuat- 
ing. Sometimes one sees a chronic wound or fistula in 
these foci which presents a stinking secretion indicative of 
gangrene. The nodular foci develop slowly. 

At first the quantity of milk is only slightly lessened, 
but later very much diminished. In quarters which have 
not undergone very marked changes the milk is of almost 
normal appearance. Later when they have' become more 
extensively altered the milk shows clumps of pus, since the 
milk is mixed with pus, and finally it is yellow, thick and 
purulent and contains free fibrin shreds. In secondary 
infections the milk can become grayish-red, and in gan- 
grene it has a foul odor. The odor is often characteristic 
and it is specific for pyobacillosis. It resembles rotten 
cabbage. 

Upon microscopical examination of the sediment one 



84 MASTITIS OF THE COW 

usually perceives a great number of Gram positive pyog- 
enes bacilli outside of the cells. 

When uncomplicated the condition is free from fever, 
but passes on to chronic emaciation with leather-like thick- 
ening of the skin and roughened hair coat. In complica- 
tions with secondary infections or (and) with gangrene 
fever develops which may be high and continuous. 

The above mentioned case with localization of the in- 
fection principally in the cisterns and milk-ducts presents 
a somewhat diverging picture. The affected quarter is 
uniformly swollen and hard. The milk is perhaps of 
normal appearance or may show fibrin flakes. The quan- 
tity of milk decreases somewhat slowly and tends to ter- 
minate after one to two months, or longer, by complete 
suppression of milk secretion. 

Prognosis is always unfavorable. Healing of this 
udder condition is possible but very infrequent. A pro- 
gressive destruction of the organ is the rule. The affection 
predisposes to fatal complications with secondary infections 
and gangrene. With manifestation of such conditions, 
high fever and red-stained or stinking milk, the prognosis 
is unfavorable. 

Treatment. — Prophylaxis is the most important. If 
a stable of cows contains one case of udder-pyobacillosis one 
should slaughter the affected cow in order to prevent fur- 
ther spreading of the infection. If the owner will not con- 
sent to this the animal must be strictly isolated. She is 
milked last and the infected milk must be so treated with 
disinfectants that the living infectious organisms cannot be 
further distributed. For prevention of a possible trans- 
mission of the infection by means of flies, the teats and 
wounds, if wounds be present, of the affected cow may be 
smeared with creolin-petrolatum, which the flies avoid 
because of its odor. 

By actual treatment one endeavors, when possible, to 



UDDER-PYOBACILLOSIS 85 

bring about a sclerosis and atrophy of the affected quarter. 
In this way the progressive destruction of the udder is 
prevented, healing is possible and at the same time the udder 
becomes less susceptible to secondary infections. 

Deep point firing or cautery in a completely infected 
quarter is indicated since the treatment greatly favors 
sclerosis and contraction. 

If fluctuation is observed the abscess is opened with a 
scalpel, the pus emptied, and the inside of the cavity thor- 
oughly cauterized with a cautery iron. 

If a secondary milk-infection [parenchymatous mas- 
titis] is complicated with it, this is additionally treated with 
injections of boric acid solution and inflation with air. If 
indications point toward death of the animal one may 
possibly attempt to prevent it by extirpation of the diseased 
half of the udder. 

In gangrene accompanied by high fever one can ampu- 
tate the teat in order to induce free drainage of the secretion. 

In fever a febrifuge like camphor is indicated. 

Summary 

I. Infectious organism : the bacillus pyogenes. 
Characteristics. 
Occurrence. 
Morphology. 
Cultivation. 
Res is tan cy. 
Pathogenicity. 
II. Udder-infection. Udder-pyohacillosis. 
Stroma-infection [interstitial mastitis]. 
Ports of infection. 
Local conditions. 
Forms : 

1. Primary udder-pyobacillosis. 
a. Through teat-infection. 
h. Through wound-infection. 



86 MASTITIS OF THE COW 

2. Secondary or embolic udder-pyobacillosis. 

Secondary milk-infection [parenchymatous mas- 
titis]. 
Secondary infections. 

1. Milk-infection [parench^^matous mastitis]. 

2. Stroma-infection [interstitial mastitis]. 
a. Acute or wound-infection. 

h. Chronic. 
Saprophytic invasion. 

1. Milk-gangrene. 

2. Wound-gangrene. 
General conditions. 

Blood-infection. 

Intoxication. 
Termination. 
Clinical symptoms. 
Prognosis. 
Treatment, 



CHAPTER X 

UDDER-TUBERCULOSIS 
Infectious Organism 

The infectious organism is the tubercle bacillus, bacillus 
tuberculosis. This bacillus is well known and therefore I 
shall omit its description. 

I will mention, however, that this organism differs from 
the preceding in that it is a strict parasite and therefore 
its occurrence is confined to the animal host. It has a very- 
great geographical distribution nevertheless. In Sweden 
it is common in the southern and middle parts, but is less 
frequently found in the north. 

When excreted from the body of the host in pathological 
discharges it cannot multiply under common conditions as 
a strict parasite. Although it does not form spores it does, 
however, obstinately resist harmful external influences as 
drying or mixing with other bacteria like those of putre- 
faction, and it may live for a month in dark places and 
retain its virulence. 

Transmission of the infectious organism does not de- 
mand direct contact of one animal with another, but can 
be brought about by objects like straw which have become 
contaminated by pathologic discharges containing the tu- 
bercle bacilli. Indirect transmission, indeed, seems to be 
the most common. 

I have never inoculated a cow's udder with tubercle 
bacilli, but with an experiment one could depend upon the 
same conditions as those obtained in the experiment with 
bacillus pyogenes, i.e., that the bacilli are taken up by the 
leucocytes through which the milk becomes free from the 
bacilli, and after one week, fourteen days or longer after 

87 



88 MASTITIS OF THE COW 

the infection, bacilli again appear in the milk. That is to 
say, the tubercle bacillus like the bacillus pyogenes is a 
typical cell parasite. 

Udder-infection 

Udder-infection is not altogether infrequent. Figures 
taken from statistics on tuberculosis in the Malmoer slaugh- 
ter houses for 1905 showed ca. 3.5 per cent, of tuberculous 
cows to be affected with udder-tuberculosis. 

The tubercle bacillus always presents a typical stroma- 
infection which can, however, develop into a secondary milk- 
infection by ulceration of the milk-canals. Stroma-infec- 
tion is thus of the greatest importance. 

STEOMA-iNFECTiON [Interstitial Mastitis^ 

This infection has a typical chronic and progressive 
character. 

Ports of Infection. — The infection can enter through 
the teat canals, through wounds or through the blood. 

The infection through the blood is the most common. 
It is one which follows tuberculosis of the lungs with blood- 
infection following ulceration of veins. 

If a blood-infection is produced by any other organ 
following ulceration of a vein or through transportation 
by lymph through the thoracic duct, the infectious organ- 
isms as a rule are picked up in the lung capillaries by the 
leucocytes and carried into the lung tissue, by which process 
the blood is freed from the organisms. It is, however, pos- 
sible that one or more bacilli may not be carried into the 
tissue of the lung, but pass through the lung and through 
the pulmonary veins, ultimately reaching the blood of the 
aorta and thus perhaps be carried to the udder. Thus it 
is possible, although not frequent, that infection of the blood 
of the udder is caused by tuberculosis in organs other than 



UDDER-TUBERCULOSIS 89 

the lungs. In such cases the foci in the lungs and in the 
udder are of the same age, the former more numerous than 
the latter, however. 

As a rule, infection of the blood in the udder is caused 
by tuberculosis in the lungs. Only exceptionally is udder 
tuberculosis caused by tuberculosis in other organs, in which 
the udder- and lung-infection occur at the same time. 

Infection through wounds is infrequent. I have only 
seen one case of this kind. The wound becomes infected by 
contamination with tuberculous products, such as coughed- 
up tuberculous mucus. The contamination can be trans- 
mitted by straw or the fingers of the attendants. 

Infection through the teat catml is less frequent than by 
way of the blood stream, but more common than the wound 
infection. The latter comparison is only natural, since the 
teat canal is always present while udder wounds are some- 
what infrequent. 

It is unreasonable to think that tubercle bacilli which 
grow so very slowly can develop in the milk of the teat 
canal, but one must consider that the infectious organism is 
mechanically forced into the teat canal on a straw, for ex- 
ample, which has been contaminated by coughed-up tuber- 
culous mucus. 

If the udder is engorged with milk the distended teats 
will be as firm as wood and the teat canals will be somewhat 
widened as a result of this distention. Thus a hard straw 
may be forced into the teat canal by movements of the 
animal while lying down. 

Another possibility of infection is by the leucocytes pick- 
ing up the infectious organisms and carrying them into the 
udder. This, however, always necessitates contamination 
of the point of the teat by tuberculous products either 
directly or indirectly by straw or by the hand of the milker. 

Local Condition. — The lesions are in proportion to 
the infectious material taken into the udder. The bacilli 



90 MASTITIS OF THE COW 

are taken up by the leucocytes in the blood, in wounds or 
in the milk and carried into the lymph spaces of the stroma, 
where the leucocytes are finally killed by the bacilli con- 
tained within them. 

Primary Lesion and Inflammation. — Around these 
necrotic cells which constitute the primary lesion, a number 
of cells are attracted, in the process of inflammation, and 
around these a layer of new connective tissue forms. This 
structure is the primary tubercle. 

By progressive necrosis a figure called a giant cell is 
formed in the centre. It is this round 
or oval necrotic focus which presents 
a zone of cell nuclei upon its external 
border which are not destroyed by the 
organism within its structure. The 
necrotic focus thus resembles a large 
cell with many nuclei, giving rise to 
Fio. 23 —Tuberculosis of the namc giant cell (Fig. 23). The 

the udder. Stronia-infection . i.'i ••i-ii ii i 

[interstitial mastitis). Primary orgamsms multiplv Within thc tubcrcle 

cell necrosis and two giant cella ^^ . _ x •' 

in the intralobular connective VCrV SlOWlV, 
tissue with corresponding in- J J ' 

X"an°d''wrofcoirc^i;; [H. F. Smyth, in his work on 
dronstrS Yn%h:"aJe:Tf tissuc culturc, has shown that tissue 
necrosis with bacterial stains, jnoculatcd with tubcrclc bacilli and 

grown in vitro will form giant cells by fusion of epithelioi- 
dal cells. The giant cells are forty or fifty times larger than 
epithelioidal cells. Giant cells may be seen anywhere in a 
tubercle, which usually presents a centre of cheesy necrosis 
surrounded by a zone of epithelioidal cells, outside of which 
is a zone of lymphocytes, which is later surrounded by a 
layer of connective tissue.] 

Distribution. — The infection manifests a great ten- 
dency to spread. A few bacilli in the primary tubercle 
may be picked up by leucocytes and be carried further into 
the stroma in the direction of the lymph stream where these 
leucocytes may be destroyed by the organisms and daughter 




UDDER-TUBERCULOSIS 91 

tubercles be produced. This is local metastasis or extension 
by leucocytes. 

In this manner the organisms can gain entrance to the 
Ijinph-vessels and be carried to the supramammary lymph- 
glands, where the degenerated leucocytes are retained and 
a tubercle is produced. Thus tuberculosis of the lymph- 
glands depends upon infection of the lymph and the process 
is therefore called lymphogenous metastasis. 

Tuberculosis in the lymph-glands following such lym- 
phatic metastasis is more recent than the tuberculosis of the 
udder. Thus we may have distinct caseation in the udder, 
but subsequent caseation in the lymph-glands may fre- 
quently be so insignificant that it is not visible to the naked 
eye. 

From these lymph-glands leucocytes may carry the or- 
ganisms through the lymph to the lumbar-glands and from 
here by way of the thoracic duct to the blood stream, by 
which it may finally be widely distributed. Thus lymphog- 
enous metastasis may be transformed into haematogenous 
metastasis. 

Besides these forms of metastasis it may also be trans- 
ported through milk [galactogenous metastasis] and blood, 
which will be discussed in another chapter. 

Development of the Tubercle. — The primary tu- 
bercle manifests slow development. Central necrosis pro- 
gresses gradually. During the lactation period, however, 
the tubercle develops somewhat rapidly in the succulent 
stroma while it develops very slowly in the alactiferous 
udder. 

Adjacent primary tubercles may coalesce by extension. 
Their connective-tissue walls and cellular zones join first 
and finally the necrotic centres coalesce and form a large 
area of necrosis surrounded by a wider zone of lymphoc\i;es 
and connective tissue. By coalescence of a large number 



92 MASTITIS OF THE COW 

of primary tubercles a very large necrotic nodule may be 
formed. 

Secondary Alterations of the Necrotic Mass. — 
This necrotic mass, which is yellowish-white in color and 
is firm and caseous through coagulation, can undergo cer- 
tain changes. 

It can become swollen and softened and be transformed 
into a pulplike mass by the imbibition of lymph, made pos- 
sible during the lactation period by increased blood- and 
lymph-supply to the organ. 

Under reverse conditions, that is scarcity of lymph, 
as in the alactiferous udder, they can become dry, firm and 
finally by resorption of liquid and infiltration of calcium 
salts become partially calcified. The calcification begins in 
the centre of the necrosis and progi'csses toward the periph- 
ery. Thus, through resorption of liquid and calcifica- 
tion, the area of necrosis forms a concrement which is 
situated in the tissue of the stroma. This concrement may 
be called a tissue concrement to distinguish it from the liquid 
concrements which are formed in milk, urine, bile and other 
fluids. 

In the softening of an area of necrosis during a reverse 
process, sandlike granules or sediment may form in the 
pulplike necrotic mass, due to infiltration of lime. 

Disturbance of Circulation by Tubercles. — Since 
tubercles are situated in the lymph-spaces of the connective 
tissue, they finally obstruct the circulation of lymph if they 
occur in great numbers. The lymph stagnates in the 
lymph-vessels in the most posterior portions of the hind 
quarters of the udder. In this manner oedema is produced 
in the quarter affected, likewise in the entire half of the 
udder, following tuberculosis of the supramammary lymph- 
glands. In this condition these glands and finally the 
lumbar-glands become oedematous. 



UDDER-TUBERCULOSIS 93 

Disturbance of Milk Excretion by Tubercles. — 
The tubercles usually form in the lower parts of the udder 
and as they develop exert pressure upon the walls of the 
adjacent milk-ducts, inducing their collapse, obstruction of 
milk flow and finally milk stasis [galactostasis] in the su- 
perior parts of the udder. The tubules and finally the 
lobules are distended by the stagnated milk. Milk con- 
cretions may form in the dilated closed tubules through 
resorption of water and precipitation of the less soluble 
matter. These are exceptionally small granules which are 
only visible with the microscope. They resemble granules 
of starch in appearance and therefore are called corpora 
amylacea. 

Milk stasis is seldom severe enough to induce pressure 
atrophy, and finally rupture of the walls between tubules 
to the formation of one large single tubule or milk cyst 
[galactocele] by coalescence of two or more tubules. 

Ulceration of Milk-ducts. — Tubercles may destroy 
the walls and epithelium of the milk-ducts. Direct contact 
with the milk increases the liquid content of the tubercle 
and in this way the necrotic area undergoes softening and 
parts of it are finally emptied into the milk. 

In this way the tubercle bacilli, like the pyogenes 
bacilli: (1) may be excreted with the milk; (2) be trans- 
ported to other parts of the same quarter by leucocytes, or 
(3) cause a secondary milk-infection by remaining in the 
milk-ducts with the thick pulp-like mass of softened necrotic 
material. 

The retained infectious organisms gradually induce ne- 
crosis of the mucous membranes, which desquamate and, 
like croupous membranes, are excreted with the milk. The 
wound produced by desquamation of these necrotic cells 
can become infected and thus the condition proceeds. 

Ulceration of a Blood-vessel Wall. — A tubercle 
can destroy a vein wall in a similar manner. The altered 



94 MASTITIS OF THE COW 

vein wall usually induces a thrombotic process, however^ 
which, as a rule, prevents infection of the blood. Ulcera- 
tion finally occurs, however, in the larger veins which are 
not occluded by the thrombus. In this case the thrombus 
is broken up by the softened tuberculous necrosis which is 
ultimately emptied into the blood stream. In this way a 
secondary blood-infection is produced which metastasizes 
to the lungs. 

Blood-infection in consequence of this thrombotic proc- 
ess always occurs later and on a smaller scale than the milk- 
infection described. 

Great numbers of such venous thrombi cause venous 
stasis with subsequent transudation by which the oedema, 
which has already been caused by lymph stasis, is increased. 

Arterial walls may be destroyed in the same manner, 
following which the condition may be more widely dis- 
tributed by infection of the arterial blood. 

Tuberculous Wounds. — If the tuberculous lesions lie 
near the skin, they may ultimately cause its necrosis and 
the softened tuberculous necrotic substance may be dis- 
charged from the wound so formed. This is somewhat 
rare. 

If the tuberculous processes lie adjacent to a primary 
wound or a secondary wound produced by ulceration, the 
tuberculous processes may ulcerate into these wounds. 

Types. — Depending upon the ports of infection, as in 
pyobacillosis, the following forms of udder-tuberculosis are 
distinguished: (1) primary udder-tuberculosis; (a) by in- 
fection through the teat canal; (h) by infection through 
wounds; (2) secondary or embolic udder-tuberculosis. 

These types have the same differential characteristics 
in general as the forms of pyobacillosis described. 

Primary udder-tuberculosis following teat infection is 
comparatively rare. Of 137 cows which had udder-tuber- 
culosis, slaughtered at the expense of the state, nine, or 



UDDER-TUBERCULOSIS 95 

6.6 per cent., did not show tuberculosis of the lungs, accord- 
ing to the post-mortem protocol. These were cases of pri- 
mary udder-tuberculosis which were obviously caused by 
infection through the teat canal, since the udders presented 
no wounds. 

Since this type of primary udder-tuberculosis can be 
present along with tuberculosis of the lungs, this figure is 
somewhat too small. It should probably not be too much 
increased, however. If we estimate, that ca. 10 per cent, 
of all cases of udder-tuberculosis are primary and caused 
by infection through the teat canal I believe that we shall 
be more nearly correct. 

It is absolutely impossible to distinguish primary from 
embolic tuberculosis of the udder by post-mortem examina- 
tion. Primary tuberculosis following infection through the 
teat canal presented no specific post-mortem picture, but 
the lesions are the same as those of embolic udder 
tuberculosis. 

Likewise, localization of lesions in one quarter is of 
no special significance, since embolic tuberculosis can begin 
in any quarter. Further, it appears that the condition can 
easily spread from one quarter to another by teat-canal 
infection. The infection can also be extended by the lymph 
stream, but only in the direction in which the lymph flows 
from the fore quarters toward the hind quarters. 

Of the nine cases of primary udder-tuberculosis induced 
by teat-infection named, five cases showed only one quarter 
affected: the left posterior quarter in two cases; the left 
anterior quarter in one case ; the right posterior quarter in 
two cases ; three cases showed two quarters affected : both 
posterior quarters in two cases ; the left posterior and right 
anterior quarter in one case; one case showed all four 
quarters affected. 

Primary Udder-tuberculosis by Infection of Wounds, — 
This is exceptionallj^ rare. I have only seen a single case 



96 MASTITIS OF THE COW 

of this kind. According to reports, the udder of the cow 
had been hooked, inducing a wound. The wound gave rise 
to a fistula. A number of tubercules were produced in the 
walls of the fistula and adjacent udder-tissue which were 
very similar in character. 

Secondary or Embolic Udder-tuberculosis. — This type, 
as before stated, is the most common and constitutes ap- 
proximately 90 per cent, of all cases. 

In 115 cases of udder-tuberculosis with synchronous 
lung- tuberculosis, that is in 115 cases which were exclusively 
of the embolic type of udder-tuberculosis, the condition is 
designated in the different quarters in the following 
manner : 

A. In one quarter : 

In left posterior quarter. . . 28 udders, i.e., 23 per cent, of cases 
In left anterior quarter. ... 5 udders, i.e., 5 per cent, of cases 
In right posterior quarter. 16 udders, i.e., 14 per cent, of cases 
In right anterior quarter . . 5 udders, i.e., 5 per cent, of cases 

Summary 54 udders, i.e., 47 per cent, of cases 

B. In two quarters: 

In both posterior quarters . 13 udders, i.e., 11 per cent, of cases 

In left posterior and ante- 
rior quarters 6 udders, i.e., 5 per cent, of cases 

In right posterior and an- 
terior quarters 13 udders, i.e., 11 per cent, of cases 

In left posterior and right 

anterior quarters 2 udders, i.e., 2 per cent, of cases 

In right posterior and left 

anterior quarters 4 udders, i.e.t 4 per cent, of cases 

Summary 38 udders, i.e., 33 per cent, of cases 



UDDER-TUBERCULOSIS 97 

C. In three quarters : 

In both posterior quarters 

and right anterior quarter 5 udders, i.e., 4 per cent, of cases 
In both posterior quarters 

and left anterior quarter 7 udders, i.e., 6 per cent, of cases 
In both anterior quarters 

and in left posterior 

quarter 1 udder, i.e., 1 per cent, of cases 

In both anterior quarters 

and in right posterior 

quarter 2 udders, i.e., 2 per cent, of cases 

Summary 15 udders, i.e., 13 per cent, of cases 

D. In all four quarters 8 udders, i.e., 7 per cent, of cases 

Totals 115 udders 

The quarter most frequently affected according to the 
following table. 

In the above named 115 cases tuberculosis occurred: 

A. In left posterior quarter. . .70 udders, i.e., 61 per cent, of cases 
In left anterior quarter ... 33 udders, i.e., 29 per cent, of cases 
In right posterior quarter . 68 udders, i.e., 59 per cent, of cases 
In right anterior quarter. .36 udders, i.e., 31 per cent, of cases 

B. In left half of the udder. . .81 udders, i.e., 70 per cent, of cases 
In right half of the udder . . 76 udders, i.e., 66 per cent, of cases 

Note: 
Exclusively in left half of 

udder 39 udders, i.e., 34 per cent, of cases 

Exclusively in right half of 

udder 34 udders, i.e., 30 per cent, of cases 

C In one or both posterior 

quarters 105 udders, i.e., 91 per cent, of cases 

In one or both anterior 

quarters 58 udders, i.e., 50 per cent, of cases 

Note: 
Exclusively in posterior 

quarters 57 udders, i.e., 50 per cent, of cases 

Exclusively in anterior 

quarters 10 udders, i.e., 9 per cent, of cases 

7 



98 MASTITIS OF THE COW 

The left half of the udder is somewhat more severely 
exposed to the infection than the right. The posterior 
quarters are much more frequently infected than the an- 
terior quarters. The anterior quarters are seldom infected. 
Usually one or two quarters, not frequently more than that, 
are affected. 

Embolic tuberculosis of the udder occurs in one of the 
posterior quarters as a rule, and in addition to it, in the 
anterior quarter on the same side, or the other posterior 
quarter or in both of these, i.e., both posterior quarters 
together with one anterior quarter. Less frequently there 
are infected only one of the anterior quarters, or one pos- 
terior quarter and the anterior quarter on the opposite side, 
or all four quarters together. 

Lung-tuberculosis in calves is somewhat infrequent, but 
is common in old cows. One may expect, therefore, that 
udder-tuberculosis will occur principally in old animals. Of 
72 cases of udder-tuberculosis : 1 animal ( 1 per cent. ) was 
3 years old; 11 animals (15 per cent.) were 4 to 6 years old; 
60 animals ( 84 per cent. ) were 7 years old or older. 

Secondary Infection by Teat-infection. — This is com- 
paratively rare, but can occur nevertheless. A complica- 
tion with chronic streptococcic infection appears to be the 
most common. Its effect is such that the milk becomes 
quickly altered and pus-like. This condition induces a 
severe sclerosis which is inhibitive to the extension of 
tubercles. In such an udder a few small tubercles are 
observed in the indurated parts, while the surrounding 
portions, which have not been affected by the streptococcic 
infection, present numerous large tubercles. 

Acute milk-infection [parenchymatous mastitis], like 
acute streptomycosis, staphylomycosis and colibacillosis, 
may develop secondarily in chronic udder-tuberculosis and 
then conceal the primary chronic condition by its intensity^ 
This complication appears to be quite rare. 



UDDER-TUBERCULOSIS 99 

Frequently secondary pyobacillosis develops wherein 
the organisms which produce an effect similar to that of the 
tubercle bacilli in general concur in the destruction of the 
udder. 

I have never observed a secondary infection with actino- 
mycosis. 

Once I observed a secondary infection with an organism 
closely allied to the diphtheria bacillus (and b. pyoneph- 
ritidis bovis) . The bacillus was Gram positive, moderately 
large, and when grown on coagulated blood serum showed 
granular inside bodies capable of taking a deep stain. Cul- 
tures in serum-gelatin-agar plates, stab serum-gelatin-agar, 
coagulated blood-serum, and in milk and bouillon were 
like the diphtheria bacillus, yet no pellicle was formed on 
the surface of the bouillon. One cubic centimetre of an 
eight-day bouillon culture injected subcutaneously killed 
a guinea-pig by intoxication. 

In addition to numerous small tuberculous foci near the 
base of the teats the udder presented five grayish-red firm 
necrotic foci ranging in size from a hazelnut to a walnut 
and surrounded by a connective-tissue capsule. Besides 
tubercle bacilli, these nodules showed a great number of 
the above-mentioned bacilli. I have never seen this con- 
dition occur as a single infection of the udder. 

Secondary Infection Through Wounds. — These sec- 
ondary infections occur from a primary wound or from a 
secondary wound produced by ulceration. Such wounds 
produced by tuberculous ulceration are rare, however. 

These secondary infections may be streptomycosis, sta- 
phylomycosis, colibacillosis and pyobacillosis. They may 
occur separately or several together. 

Staphylomycosis liquefies the necrotic area and conse- 
quently induces an infectious softening. 

Saprophytic invasion can cause milk-gangrene and 
wound-gangrene . 



100 MASTITIS OF THE COW 

Milk-gangrene does not appear to occur in simple 
udder-tuberculosis. 

I have only seen a few cases of milk-gangrene in udder- 
tuberculosis and they were complicated with pyobacillosis. 

Wound-gangrene presupposes a tuberculous wound. 
In this kind of wound gangrene is the rule. It develops 
into putrid liquefaction and softening of the necrotic tuber- 
culous area. 

General Conditions. — Blood-infection. — Tuberculo- 
sis of the udder can induce an infection of the blood-stream 
by lymphogenous transportation or by ulceration of a vein 
with subsequent metastasis to the lungs, from which point 
the condition can be more widely distributed. 

Udder-tuberculosis, which is usually caused by lung- 
tuberculosis, can finally increase the severity of the con- 
dition in the lungs by metastasis. 

Intoxication. — Like all tuberculosis of cows, udder- 
tuberculosis produces no distinct initial general symptoms. 

The animal emaciates gradually and shows anasmia, de- 
creased appetite and frequently leather-like thickening of 
the skin and roughened hair coat. 

Finally the ansemia and emaciation become so advanced 
that the animal dies. 

Complication with acute secondary infection can induce 
high fever and thus bring about death of the animal. Com- 
plication with gangrene is often accompanied by persistent 
fever. 

Termination. — Udder- tuberculosis causes a gradual 
progressive destruction of the udder-tissue, which may re- 
quire from a month to a year. Destruction progresses 
rather rapidly during the period of lactation, but more 
slowly, often very slowly, during the non-lactating period. 

Clinical Symptoms. — The condition is a chronic one 
and usually affects older cows which are 7 years old or 
older. 



UDDER-TUBERCULOSIS 101 

One or more quarters are involved and of these at least 
one of the posterior quarters. The affected quarters are 
enlarged, especially in the inferior parts. Usually the en- 
largement is uniform, seldom irregular, in which latter cases 
nodular foci are present. The enlarged portion is hard and 
painless. These portions may infrequently present a 
wound which is chronic and contains a stinking, soft, 
caseous, purulent secretion. 

The lymph-gland of the affected quarter is correspond- 
ingly increased in size. Only in one case was the lymph- 
gland not visibly enlarged. 

The quantity of milk is at first slightly but later greatly 
diminished. The milk is of normal appearance in low- 
grade alterations of the udder, but gradually changes with 
the progression of the disease. It becomes yellow and 
mixed with pus and finally yellowish-gray and purulent. 
Usually, however, it is thin and contains a few free fiocculi 
of fibrin. 

This alteration of the milk can occur rather quickly. 
After one month the milk can become distinctly changed. 
Usually, however, this does not occur until after two 
months. There are cases, however, in which the milk had 
retained its normal appearance until four months after the 
inception of the condition. These differences naturally 
depend upon the degree of distribution and the rapidity 
of development of the tuberculous lesions. 

In the rather infrequent complications with secondary 
infections or saprophytic invasion the milk can become 
grayish-red, especially in the more acute secondary infec- 
tions, and stinking in gangrene. 

Upon microscojncal examination of the sediment one 
usually finds a moderate number of acid-fast tubercle bacilli 
outside of the cells. 

With a moderate number of tubercle bacilli I believe 
that one may find from one to ten bacilli in every field when 



102 MASTITIS OF THE COW 

a uniform smear of the material is made on the slide and 
the organism is enlarged 550 times. 

The content of tubercle bacilli may vary distinctly, 
however. There are cases where from 100-200 tubercle 
bacilli occur in each field (Fig. 24), and also where the 
tubercle bacilli are exceptionally few, one in every five 
fields, one in a smear or even less, so that a microscopical 
diagnosis is made with great difficulty or not at all. 

The milk can also contain other acid-fast rods besides 
tubercle bacilli. They may be acid-fast actinomyces rods 
in udder-actinomycosis or saprophytic acid-fast rods in pol- 
lution of the milk. These rods may be mistaken for 
tubercle bacilli or, on the contrary, tubercle 
bacilli may be mistaken for these acid-fast 
rods, especially in severely contaminated 
milk samples. 

Of 841 milk samples examined micro- 
scopically here in the High School, tubercle 
bacilli were demonstrated in 155 cases, or 

Fig. 24.— Tubercle , 

bacilli in milk sedi- ^g per ccut. oi thc samplcs. 

ment. Ziehl (X 550). i p n • • j 

The followmg errors were committed: 
In two cases (0.24 per cent.) no tubercle bacilli were 
found in obstinate udder-tuberculosis. In one case the milk 
was examined again at fourteen-day intervals without re- 
sults. The udder showed a slight distribution of tuber- 
culosis without visible caseation in one anterior quarter. 
The foci contained a few tubercle bacilli. The milk caused 
tuberculosis in guinea-pigs. In the second case the milk 
was only examined once. A possible error in staining is 
not to be completely disregarded. The udder showed a few 
tuberculous caverns containing loose caseous necroses which 
were the size of a nut. In the necrotic areas a moderate 
number of tubercle bacilli were found. Perhaps more 
errors of the same kind were made, but they attained a very 
small number, perhaps fifteen of the samples examined. 




UDDER-TUBERCULOSIS 103 

In two cases (0.24 per cent.) actinomycotic rods were 
taken for tubercle bacilli. The udder showed no tubercu- 
losis, but extensive actinomycosis. 

In two cases (0.24 per cent.) acid-fast rods were mis- 
taken for tubercle bacilli. The udder was now examined 
and found to be free from tuberculosis. 

In one case (0.12 per cent.) tubercle bacilli were present 
but mistaken for acid-fast rods, since the sample was very 
badly contaminated. A new sample was sought, but not 
obtained, since the cow had been sold in the meantime. A 
guinea-pig was inoculated with the milk and developed 
tuberculosis. In at least two other cases the same condition 
was present, but the tubercle bacilli were found in the new 
samples obtained. 

Later two cases were confused with pyogenes bacilli. 
The udder, when examined, showed no tuberculosis, but 
extensive pyobacillosis. Both of these milk samples, ac- 
cording to my report, had presented a few tubercle bacilli, 
which were very few, however, as only one tubercle bacillus 
was found in two smears. Both samples contained numer- 
ous pyogenes bacilli. Frequently a few pyogenes bacilli 
were not decolorized and had been mistaken for tubercle 
bacilli. 

The rather quick microscopic diagnosis of udder-tuber- 
culosis gives very good results in spite of a few possible 
errors. 

These errors may be eliminated to a great extent by 
observing the following rules: 

1. The milk samples should only be taken from the 
affected quarter or quarters. All the milk possible is re- 
moved from the diseased quarter; in this way the bacillary 
content is the greatest. If the quantity of milk is great, 
the milk sample can stand for half an hour, when the upper 
part may be poured off and the remainder, which contains 



104 MASTITIS OF THE COW 

a rich sediment, is sent in for examination. The milk 
sample naturally should not be strained or filtered. 

2. One should avoid precipitation in the milk. Casein 
precipitation occurs in acid fermentation. This is pre- 
vented, especially in summer, when the milk easily becomes 
sour, by the addition of an antiseptic, such as boric acid, 
which does not alter the milk. Addition of chloroform is 
not indicated, since chloroform induces precipitation of the 
fat. The precipitations cause the smear to be poor in 
bacilli and lessen the possibility of finding the tubercle 
bacilli. 

3. If the result of the examination is negative a new 
sample of milk can be obtained after from ca. eight to 
fourteen days, which often contains more tubercle bacilli 
which are then more easily discovered. 

4. Strict cleanliness should be observed in the collection 
of milk samples. This reduces contamination with acid- 
fast organisms. 

If the condition is so old and the udder so destroyed 
that no milk can be obtained, a harpoon probe must be 
made in order to obtain a diagnosis; moreover, such a 
sample is unnecessary. 

Treatment of these conditions is not permitted in 
Sweden, according to the Royal Order of May 1, 1903. 
The animal must be slaughtered if the diagnosis of udder- 
tuberculosis is established. [No such Federal law exists 
in this country, but interstate shipment is prohibited. The 
majority of municipal laws prevent shipment of milk from 
such a cow into the municipality.] 

If the animal is suspected of udder-tuberculosis it can 
be isolated from the rest of the animals and milked last in 
anticipation of the diagnosis. Its milk should not be used 
at all for man and animals, or only after it has been boiled. 



UDDER-TUBERCULOSIS 105 

Summary 

1. Infectious organism : tubercle bacillus. 
Occurrence. 

Resistancj. 
Experimental mastitis. 

2. Udder-infection : udder-tuberculosis. 
Stroma-infection. 

Ports of infection : blood, wounds and teat canals. 
Local conditions. 
Primary tubercles. 

Distribution: regional, lymphogenous, liaematogenous 
distribution as well as distributed by the milk. 
Growth of tubercles. 

Alteration of necrosis. Colliquation and calcification. 
The tubercles cause stagnation of the blood and the milk. 
Ulceration of the milk-ducts (milk-infection). 
Ulceration of the blood-vessels (blood-infection). 
Ulceration through the skin or into wounds. 
Types : 

1. Primary udder- tuberculosis. 

a. By teat-infection. 
6. By wound-infection. 

2. Secondary or embolic udder-tuberculosis. 
Secondary infections : 

a. By the teat canals. 

b. By wounds. 
Saprophytic invasions : 

a. Milk-gangrene. 
h. Wound-gangrene. 
General conditions : 

Blood-infection. 

Intoxication. 
Termination. 
Intoxication. 
Clinical symptoms. 

Microscopical diagnosis. 

Possible errors. 

Rules for collection of milk samples. 
Treatment. 



CHAPTER XI 

UDDER-ACTINOMYCOSIS 

Infectious Organism 

The infectious organism is the actinomyces bovis or ray 
fungus. 

Characteristics. — The pathogenic actinomyces bovis 
is a small thin filamentous organism which sometimes shows 
finger-like branching and which forms round spore-like 
bodies. In the animal body it forms round radiated col- 
onies. Round finger-like or club-shaped bodies are 
arranged on the surface of the structure in a radiating 
manner and appear at the edge as a marginal zone. The 
filaments are difficult to stain, but may be stained by Gram's 
method. This fungus is exceptionally difficult to cultivate. 

Occurrence. — The actinomyces fungus appears to be 
of uniform geographical distribution. 

In Sweden it is quite generally distributed, but appears 
to be present more especially in certain known districts, 
however. 

It appears to be found on straw and bearded grains, 
since the infection is often carried by these foreign bodies. 

Morphology. — The actinomyces fungus occurs in two 
forms, filamentous and spherical. 

The appearance of the filaments varies. They may form 
single fine rods which closely resemble the tubercle bacillus, 
and may also be mistaken for tubercle bacilli. As a rule, 
however, they are somewhat thicker, show finger-like 
branching, and the branches often show swollen club-shaped 
ends. 

The spherical form or spore-like bodies (perhaps real 
spores) are somewhat uniformly round and fairly large, 
approximately the same size as the staphylococcus. 

106 



UDDER-ACTINOMYCOSIS 



107 



The fungus forms characteristic colonies in the animal 
body. These structures are yellow or yellowish-brown, 
round or irregularly shaped polygonally rounded bodies 
from 0.1 to 2 mm. in diameter. The larger colonies are 
always visible to the naked eye as yellow or yellowish-brown 
points. 

With a magnification of 30 diameters they show a homo- 
geneous wax-like appearance and a uniform or usually 
slightly crenated margin (Fig. 25) . With a greater mag- 
nification ( X 250) the margin presents a zone of radiating 
club-shaped bodies (Fig. 26). 

On cut section and with greater magnification the col- 






FiG. 25. — Actinomyces 
colonies in pus. Unstained 
preparation in saline solu- 
tion (X 30). 



Fig. 26. — Actinomyces 
colonies in pus. Unstained 
preparation in saline solu- 
tion (X 250). 



Fio. 27. — Actinomyces 
colony. Cut section. Gram. 
(X 300). Sporelike bodies 
in the centre. 



onies present a core and a radiated finger-like margin. 
The centre shows the little round spore-like bodies, and 
outside, the margin shows the finger-like divisions and club- 
shaped swollen filaments (Fig. 27). The most external 
part of the margin formed by the club-shaped rays may 
be deeply stained with eosin and picric acid. In this way 
these stains are often of assistance in searching for the 
colonies. 

The zone of club formations appears around the fila- 
ments like a protective capsule. It only occurs on the 
periphery and guards against the harmful protective in- 
fluences of the animal host. The size of these clubs varies 



108 MASTITIS OF THE COW 

considerably. They are usually small and by magnifying 
250 diameters are just barely visible. In less frequent cases 
they are quite large and may be seen by magnifying 100 
diameters. 

The fungus is very difficult to stain, is Gram positive, 
but must be carefully decolorized. The filaments are not 
infrequently acid-fast. 

Cultivation. — The fungus is exceptionally difficult 
to cultivate. I have attempted its cultivation repeatedly 
without success and therefore advise nef erence to text-books 
on bacteriology for its cultural characteristics. 

Pathogenicity. — Since I did not cultivate the organ- 
ism I performed no animal experiments. 

The actinomyces fungus is a cell parasite like the pyog- 
enes and tubercle bacilli and one may therefore reach the 
same conclusions in experiments with the actinomyces 
fungus as with the pyogenes bacillus. One may also ex- 
pect that the fungus injected into the udder will soon be 
taken up by the leucocytes and removed from the milk. 
These leucocytes carry fungus into the udder stroma, where 
fungus colonies are formed which may destroy the milk- 
ducts and finally be discharged into the milk after from 
one to several weeks. 

Udder-infection 

This is rare. The actinomyces fungus always produces 
a typical stroma-infection [interstitial mastitis]. 

STROMA-iNFECTiON [Interstitial Mastitis^ 

Like tuberculosis, this infection possesses a typical 
chronic progressive character. 

Ports of Infection. — The organism can gain en- 
trance through the teat canal, through wounds or through 



UDDER-ACTINOMYCOSIS 109 

the blood-stream. I have never seen the infection produced 
through an udder-wound. 

An infection through the blood-stream always follows 
actinomycosis of the lungs. This disease is rare, however, 
perhaps less frequent than actinomycosis of the udder. 
Therefore I maintain that this portal of entry does not 
play so great a role since I know of no positive case of 
actinomycosis of the lungs and udder together. 

The most important port of infection is the teat canal. 
Of seven actinomycotic udders sent to the Veterinary High 
School three of the cases were reported to have shown no 
alterations in the lungs. Lung tuberculosis was observed 
in one case and in the three other cases no report was made 
concerning the lungs. None of the udders presented 
wounds. 

Of four cases with complete history, therefore, three 
were positively primary udder-actinomycosis through teat 
infection. In the fourth case it may be possible that actino- 
mycosis was also present with the tuberculosis but was 
overlooked by the veterinary inspector. This case is there- 
fore probably, but not positively, primary udder-actinomy- 
cosis through teat-infection. 

It is not to be thought that the slowly growing actino- 
myces fungus develops in the milk in the teat canal, but 
one must admit, on the contrary, that the organism is 
mechanically forced into the teat canal on a straw. 

Local Conditions. — Leucocytes pick up the fungus 
and deposit it in the lymph spaces of the stroma, where the 
fungus finally destroys the leucocytes. 

Primary Lesion and Inflammation. — The fungus 
paralyzes and necrotizes the leucocytes which have engulfed 
it and this cell necrosis constitutes the primary lesion. 

A great number of cells emigrate and collect around 
the primary lesion (emigratory stage of inflammation), 
and outside this wall of leucocytes a capsule of new con- 



110 MASTITIS OF THE COW 

nective tissue forms. This structure constitutes the pri- 
mary actinomycoma (Fig. 28). 

The wall of cells of an actinomycoma often presents two 
different layers: 

1. An internal thin layer of lymphocytes showing little 
protoplasm and large round nuclei rich in chromatin. 

2. An external thicker layer of epithelioidal connective- 
tissue cells showing oval vesicular nuclei poor in chromatin, 
but with considerable protoplasm. 

In the centre of the focus the fungus gradually develops 
into a characteristic ray fungus colony. The adjacent part 
of the zone of cells surrounding the 
fungus undergoes necrosis, but this is 
corrected by the emigration of fresh 
cells to replace them. The formation 
of actinomyces colonies develops 
slowly. 

Distribution. — The infection 
„ „ . . . , shows a tendency toward metastasis. 

Fig. 28. — Actinomycosis of *' . . 

i50)"'^'^An^*ovS*''fctinimycM Mctastasis m actmomycosis is de- 
Ltor"y"iL'"^ri€oiB^i cidedly less frequent than in tuber- 

visible in the swollen intralo- /-»nlr»cic 
bular connective tissue. The LUlOaia. 

ac^nomycoma'Terira- corner Extcnsion of thc COUditioU is 

of interlobular connective tissue. • • n • i t> i j. • 

prmapally regional. J3y leucocytic 
transportation a single fungus cell of a colony forms a 
daughter actinomycoma in the neighborhood of the pri- 
mary actinomycoma. This local metastasis usually occurs 
in the direction of the lymph-stream. 

Finally the actinomyces fungus can penetrate the l}Tnph- 
vessels, be carried to the supramammary lymph-glands and 
thus by lymphogenous metastasis produce new actinomy- 
cotic foci. This metastasis to the lymph-glands appears 
to take a very long time. Of four udders received the 
lymph-glands were still attached. In only one case was 
the lymph-gland on the side of the udder affected swollen 
and actinomycotic. This udder showed very old actinomy- 




UDDER-ACTINOM YCOSIS 1 1 1 

cotic foci up to the size of a walnut, while the foci in the 
lymph-glands were the size of a pea. 

Metastasis by the milk plays a greater part and will 
be discussed later. Metastasis by the blood-stream appears 
to be quite rare. Actinomycosis of the lungs is somewhat 
infrequent, while actinomycosis of the tongue and jaws is 
common. 

Growth op Actinomycomata. — The primary actino- 
mycoma manifests a very gradual development. The 
central colony is very slowly enlarged. During the lacta- 
tion period development is more rapid, but is slower during 
the quiescent state. 

Neighboring actinomycomata, as primary foci, and their 
daughter foci may coalesce by extension and produce 
nodules ranging in size from a pea to a walnut or larger. 
These nodules are composed of soft connective tissue and 
numerous foci containing evenly distributed actinomycotic 
colonies. 

Secondary Alterations of Actinomycomata. — 
When great quantities of fluid are present, especially when 
an actinomycoma has destroyed a milk-duct and thus is 
brought in direct contact with the milk, the actinomycoma 
can soften, disintegrate, and become a viscid, purulent, 
slimy, thick fluid. 

Conversely when little fluid is present the actinomyces 
colonies develop so slowly that the connective tissue of all 
the actinomycoma proliferates very vigorously, more or less 
circumscribing the infection by encapsulation. Under such 
conditions the actinomyces colony can undergo retrogressive 
metamorphosis, become partially or entirely necrotic and 
finally be transformed into a concrement by calcification. 

Actinomycomata by their development appear to ofl'er 
an obstruction to the blood circulation and to the milk flow. 

Ulceration of Milk-ducts. — Actinomycomata may 
destroy the wall of a milk-duct. By absorption of milk 



112 MASTITIS OF THE COW 

actinomycomata may become swollen, softened and disin- 
tegrated and finally be discharged into the milk. In this 
manner the ray fungus can: (1) be discharged into the 
milk; (2) be spread to other parts of the same quarter by 
leucocytes; (3) stagnate in the milk-ducts together with 
softened necrotic parts of the actinomycoma. 

Genuine milk-infection Iparenchymatous mastitis] 
does not appear to occur; that is the stagnated fungus does 
not induce necrosis of the subjacent epithelium, at least not 
to any marked degree. Formation of croupous membranes 
does not appear to occur in this condition. 

Ulceration of a Blood-vessel Wall. — This is pos- 
sible, of course, but only appears in exceptional cases and 
with the relative infrequency of actinomycosis of the lungs. 

Ulceration Through the Skin. — I have not ob- 
served this condition in any of my cases. It is possible, 
however, like the not uncommon ulceration of the skin in 
actinomycosis of the jaw. It is certainly very infrequent 
in the udder, nevertheless. 

types 

Depending upon the ports of infection the following 
types are distinguished : ( 1 ) primary udder-actinomycosis, 
(a) by infection through the teat canal, {h) by infection 
through wounds; (2) secondary or embolic udder-actino- 
mycosis. 

These types have the same general differential char- 
acteristics as the previously described types of pyobacillosis 
( see Pyobacillosis ) . 

Primary udder-actinomycosis following teat-infection 
is the most common type. The foci are so distributed in 
the udder that one cannot expect to find an anatomical 
difference from the embolic type upon post-mortem exam- 
ination. The condition almost always begins in one quar- 
ter, but may frequently be spread to other quarters by 



UDDER-ACTINOMYCOSIS 113 

lymphogenous metastasis and by infection through the teat 
canal. In one case of distinctly primary udder-actinomy- 
cosis induced by teat-infection all four quarters became 
affected. 

Primary udder -actinomycosis following wound infection 
is a condition I have not seen, but if it occurs it certainly 
has a particular anatomical character which closely simu- 
lates the corresponding type of udder tuberculosis. 

Secondary or embolic udder- actinomycosis is a condition 
I have not observed in any of the udders that I have ex- 
amined, but that it can occur appears to be natural. 

The possible secondary infections might be strepto- 
and staphylomycosis, colibacillosis and perhaps pyo- 
bacillosis. 

Secondary infection through wounds always occurs 
through an actinomycotic wound, and here, as with all 
chronic wounds, secondary infection is the rule. Secondary 
infections which one may expect in this case are the same 
as those previously described. 

Saprophytic invasion can induce milk- and wound- 
gangrene. 

Milk-gangrene [gangrenous mastitis] does not appear 
to occur in primary udder-actinomycosis. It is possible in 
secondary infections. 

Wound-gangrene, when it occurs, always develops from 
an actinomycotic wound, and it may easily develop in this 
condition. As previously stated, a wound of this kind is 
very infrequent. 

General Conditions. — Infection of the blood with 
metastasis to the lungs is an uncommon complication. 

Intoxication. — Udder-actinomycosis usually presents 
no distinct general symptoms. If the condition is far ad- 
vanced, however, or metastatic processes have developed the 
animal may emaciate nevertheless, and finally present 
symptoms of anasmia and debility. 

8 



114 MASTITIS OF THE COW 

Termination. — Udder-actinomycosis is a typical local 
condition and causes a progressive gradual destruction of 
the udder, extending over the course of a year. 

Clinical Symptoms. — The condition is very chronic. 
The affection usually begins in one quarter, but it can 
affect other quarters by extension or by infection through 
the teat canal. The quarters affected are enlarged, espe- 
cially in their inferior portions. The increased part is hard 
and painless. 

The lymph-gland of the diseased quarter is swollen if 
the condition is an old one. Usually it is not enlarged. 

The quantity of milk gradually diminishes. The milk 
is of normal appearance for a long time, even for several 
months, but gradually becomes thin and mixed with pus 
and finally yellow and purulent, still continuing somewhat 
thin. 

Upon microscopical examination of the sediment in an 
unstained coverslip preparation made by careful isolation 
of the elements of the sediment in physiological salt solu- 
tion by the use of a needle, usually a very few, seldom 
many, actinomyces colonies were observed outside the cells. 
These actinomyces colonies are always very small and very 
spongy and frequently present a very indistinct radiating 
form. The yellow color, the rounded crenated margin, 
the homogeneous waxy condition and the cells are usually 
of great assistance in finding the colonies with low mag- 
nification (ca. 30 diameters). 

Diagnosis with the microscope is usually very difficult 
and errors may easily occur ; that is, one may find no actino- 
myces colonies after diligent search in spite of the fact that 
udder-actinomycosis is present. I have had one case of 
this kind. 

Preparations stained after the method of Gram also 
gave uncertain results. In preparations stained by the 
acid-fast method one can sometimes find a few fine acid- 



UDDER-ACTINOMYCOSIS 1 15 

fast rods which greatly simulate tubercle bacilli and which 
may also become confused with them. 

The PROGNOSIS is unfavorable for the udder. The con- 
dition continues to a progressive destruction of the udder. 

Treatment. — Prophylaxis is the most important. All 
open cases of actinomycosis of the jaw, tongue or udder 
spread the infectious organisms and in this way encourage 
the possibility of actinomyces infection and thus udder- 
actinomycosis. Slaughter of all animals showing open 
actinomycotic lesions is the safest measure to adopt in pre- 
vention of such an infection. If the owner will not consent 
to this the animals are isolated as strictly as possible and 
so treated as to disinfect the diseased products bearing the 
infectious organisms. 

Actual Treatment. — One should endeavor to induce 
sclerosis and atrophy of the infected part of the udder 
wherever possible, which prevents progressive destruction 
and encourages healing. 

The cow remains and the entire infected quarter is 
deeply point-fired with a cautery iron, which promotes 
sclerosis and contraction to a high degree. 

The treatment is completed by administering 8 to 12 
g. of potassium iodide per os daily for from three weeks 
to a month, a course which is always indicated in actino- 
mycosis. 

Summary 

1. Infectious organism: actinomyces bovis. 
Characteristics. 
Occurrence. 
Morphology. 

Filamentous form. 

Club form. 

Colonies. 
Staining. 
(Cultivation and pathogenicity.) 



116 MASTITIS OF THE COW 

2. Udder-infection: Udder-actinomycosis. 

Stroma-infection [interstitial mastitis]. 

Ports of infection : teat canals, wounds and blood. 
Local conditions. 

Primary actinomycoma. 

Metastasis : regional, lymphogeneous and hasmatogen- 

ous metastasis as well as galactogenous metastasis. 
Development of actinomycomata. 
Secondary alterations of actinomycomata. 

Softening and encapsulation. 
Ulceration of milk-ducts. 
Ulceration of blood-vessels. 
Ulceration through the skin. 
Types : 

1. Primary udder-actinomycosis. 

a. By teat-infection. 

b. By wound-infection. 

2. Secondary or embolic udder-actinomycosis. 
Secondary infection. 

1. By the teat canal. 

2. By wounds. 
Saprophytic invasion. 

1. Milk-gangrene. 

2. Wound-gangrene. 
General conditions. 

Blood-infection. 

Intoxication. 
Termination. 
Clinical symptoms. 
Prognosis. 
Treatment. 

Prophylaxis. 

Actual treatment. 



CHAPTER XII 



UDDER-NECROBACILLOSIS 



I HAVE very little to say concerning this rare affection 
of the udder since I have never seen a case. Jensen reports 
a case (Mastitis in Animals, 1899). Lucet's Case VIII 
(Mammites Aigues, 1891) is perhaps this infection, 
although negative results were obtained by inoculation of 
dogs, which was probably due to too short observation. On 
the other hand, the bacteria isolated by Steiger as necrosis 
bacilli (Bacterial Findings in Mastitis, 1904) were cer- 
tainly not bacillus necrophorus, since they were Gram 
positive, but were probably pyogenes bacilli. 

The infectious organism is the necrophorus bacillus. It 
is a somewhat fine. Gram negative, obligate anaerobic, 
thread-like bacillus which is very difficult to cultivate. It 
is pathogenic for mice and dogs and produces typical 
chronic lesions following inoculation. 

The organism appears to be a typical cell parasite, like 
the pyogenes and tubercle bacillus. 

Udder-infection 

The bacillus necrophorus produces a distinct typical 
stroma-infection [interstitial mastitis] of chronic progres- 
sive character as in the three previous udder-infections, and 
the milk-infection [parenchymatous mastitis] is only a com- 
plication of it. 

Ports of Infection. — The infection can take place 
through the blood-stream (Jensen) and probably through 
the teat canal and wounds. 

Types of the Local Conditions. — The case reported 
by Jensen was an embolic udder-necrobacillosis. 

117 



118 MASTITIS OF THE COW 

Lucet's case, which was only described clinically, was 
perhaps a primary udder-necrobacillosis through teat in- 
fection. No case of primary udder-necrobacillosis through 
wound infection has been reported in the literature available. 

Mixed Infection. — In the case described by Lucet 
streptococci were found in the exudate in addition to these 
bacilli. 



CHAPTER XIII 

CLINICAL DIAGNOSIS OF MASTITIS 

Mastitis Caused By External Force 
Bruises and wounds of the udder are easy to diagnose. 
The sclerosis following repair of an abrasion might pos- 
sibly be mistaken for a chronic udder-infection. A good 
history and careful examination of the milk are of great 
assistance in making a differential diagnosis. 

Udder-infection 

Infections of the udder may be divided clinically into 
wound-infections and specific udder-infections. 

infected udder-wounds 

These wound-infections are recognized by a more or 
less severe swelling in the neighborhood of the wound, and 
the secretion, which usually consists of yellow pus, but 
which may infrequently present a red-colored serous fluid 
in severe acute infections. 

Wound-infections may be divided into acute and chronic 
forms, depending upon the course. 

The acute wound-infections are streptomycosis, staphy- 
lomycosis, and colibacillosis. 

Wounds complicated by acute infections usually heal 
in ca. one month. The infection often begins with fever. 
At first the secretion is serous, but later becomes purulent. 
If the infection advances when the wound is fresh it may 
become complicated with an acute milk-infection. Gan- 
grene of the wound secretion is an exception. 

A clinical differentiation of the three types appears to 

119 



120 MASTITIS OF THE COW 

be impossible and is of no practical significance, since 
wound-infection is seldom treated as a single infection, but 
as a mixed infection. 

The chronic wound-infections are pyobacillosis, tuber- 
culosis and actinomycosis. 

These complicated infectious wounds show little or no 
tendency to heal, but gradually become larger. 

Fever can occur in complications with acute infections 
(mixed infection). In gangrene, fever is always present, 
otherwise these infections are free from fever. 

All these chronic infections spread into the udder-tissue, 
which often manifests a widely circumscribed hard swelling 
around the wound, together with alteration of the milk 
(see under Specific Udder-infections). 

In pyohadllosis the wound-secretion is thick and yellow, 
the consistency of cream or salve, and contains no calcareous 
granules. The walls of the wound are composed of smooth, 
firm and tough connective tissue, which is colored green 
in gangrene by pigment of putrefaction. Gangrene is very 
common. The corresponding lymph-gland is not enlarged. 

In tuberculosis the secretion is yellow, soft, caseous and 
frequently contains calcareous granules which are easily felt 
by rubbing the pus between thumb and finger. The walls 
of the wound are often irregular and nodular with tubercles. 
Gangrene is very common. The corresponding lymph- 
gland is enlarged. 

In actinomycosis the quantity of the secretion is usually 
small, qualitatively it is yellow and viscid, due to disin- 
tegration of actinomycomata. The wound may become 
filled with red, soft, spongy granulation tissue which may 
protrude from the wound as a great oval red nodular actino- 
mycoma. The wound does not heal, but gradually in- 
creases. Gangrene is not so common because of the small 
quantity of the secretion. The corresponding lymph-gland 
is usually not enlarged. 



CLINICAL DIAGNOSIS OF MASTITIS 121 

GENUINE UDDER-INFECTIONS 

These infections are manifested by changes in the udder 
and the milk. They may also be divided into acute and 
chronic forms. 

The acute genuine udder-infections are streptomycosis, 
staphylomycosis, and colibacillosis. They are severe in the 
beginning, but are seldom fatal. Usually repair is estab- 
lished by inflammation and sclerosis in a month. 

They are typical infections [parenchymatous mastitis] 
and usually begin in one quarter, but may also spread to 
other quarters by infection. Simultaneously with the in- 
fection alterations in the milk occur. In severe infections 
the milk is transformed into a serous, even red-stained, thin, 
somewhat muddy fluid secretion. On the other hand it 
may consist of thick yellow pus or a thick yellow mixture 
of pus and milk. Slimy flakes of fibrin are frequently 
present in the pus or altered milk. 

In addition to the changes in the milk a hard swelling 
of the quarter occurs at the same time, which is at first 
painful and later becomes painless and may vary to a high 
degree. The corresponding lymph-gland is but slightly 
or not at all affected. The condition usually begins with 
fever, which subsides after a few days. Complications 
with acute secondary infections and gangrene produce a 
recurrence of fever and destroy the healing process. These 
complications are rare, however. 

A specific clinical diagnosis of these affections is usually 
impossible. 

One may suspect streptomycosis if the condition is 
epizootic and affects a number of cows with a high fever 
of short duration, and high or low gi'ade disease processes 
in the udders and milk. This is especially so when the 
joints (tarsal joint) synchronously present a painful swell- 
ing. If the condition Is vigorous and severe or fatal, one 



122 MASTITIS OF THE COW 

may suspect staphylomycosis. The more common sporadic 
cases may be any of the three infections. 

The chronic genuine udder-infections may be divided 
into two groups: 

1. Atypical chronic udder-infections which begin as 
severe acute infections and then become chronic. 

2. Typical chronic udder-infections which are not 
noticeable in the beginning. 

Atypical udder-infections are undoubtedly strep tomy- 
cosis. 

The atypical chronic streptomycosis begins with all the 
symptoms of a severe acute udder-infection (milk-infec- 
tion) [parenchymatous mastitis] with alterations of the 
milk, swelling of the udder and fever. The fever subsides, 
but the alterations of the milk and swelling of the udder 
remain about a month. The udder finally becomes as 
hard as stone, through sclerosis, and may manifest nodular 
foci which, when incised, present pus and probably firm 
necrotic sequesters in an abscess cavity surrounded by a 
smooth connective-tissue wall. 

Pyobacillosis and tuberculosis may run a course like an 
atypical chronic udder-infection when they enter an acute 
udder-infection as complicating secondary infections. In 
these cases the acute infection is simply displaced by a 
different chronic infection. 

Typical chronic udder-infections are not noticeable in 
the beginning, but gradually produce alterations in the milk 
and udder. 

When a blood-vessel is injured the milk may be slightly 
tinged with blood. The lesions of the udder are but slightly 
or not at all painful. 

These infections may be divided into two sub-groups: 
(a) those which cause a distinct swelling of the udder; 
(&) those in which no distinct swelling is present. 

The typical chronic udder-infections which cause a dis- 



CLINICAL DIAGNOSIS OF MASTITIS 123 

tinct swelling of the udder are the typical stroma-inf ections : 
Pyobacillosis, tuberculosis, and actinomycosis. 

The swelling of the udder is the first distinct symptom 
of the disease. At first the milk is not changed, then it 
becomes mixed with pus and finally, in about a month, 
purulent. 

In order to observe the lesser changes in the milk, the 
diseased quarter is well milked out and the milk poured 
into a litre flask made of uncolored glass. The flask is 
stoppered and then inverted for ten or fifteen minutes. At 
the end of this time the sediment has collected in the neck 
of the flask and on the stopper, so that one may readily 
examine it for quantity, color and other qualities. 

Pyobacillosis usually aff'ects but one quarter, but may 
spread to other quarters by infection. It produces a mod- 
erate and finally large hard swelling of the udder. The 
corresponding lymph-gland is not swollen. 

The milk frequently has a normal appearance, but 
contains pus. It gradually becomes more intensely altered 
and finally, after months, the milk becomes purulent, thick 
and pulpy in consistency, due to the presence of thicker 
pus. Gangrene is a common complication and imparts a 
foul odor to the milk, which assumes a characteristic stink, 
specific of decomposed cabbage. 

If the condition is an old one abscesses may form in the 
udder which contain yellowish-green, thick, pulpy pus. 
These may rupture upon the external surface and produce 
fistulae. 

The condition is free from fever in the beginning, but 
it occurs following the frequent complications with acute 
secondary infections and gangrene. 

Tuberculosis attacks one or more quarters. The swell- 
ing is very large and hard. The corresponding lymph- 
gland is always enlarged and sometimes very greatly so. 

The size of the lymph-glands is different in the different 



124 MASTITIS OF THE COW 

cows, but in the same animal both supramammary lymph- 
glands are the same size under physiological conditions. 
Thus a unilateral lymph-gland swelling is easy to deter- 
mine, while, on the other hand, bilateral swelling is often 
difficult. 

At first the milk is normal in appearance, later becomes 
mixed with pus and finally, after a period of several months, 
is pui'ulent. In this condition it is composed of a yellow, 
serous, thin pus containing flakes of fibrin. Milk-gangrene 
is exceptionally rare. 

Secondary infections and abscess formation are very 
infrequent. The contents of the abscesses when they do 
occur is made up of yellowish-white, soft, caseous pus con- 
taining calcareous granules. The condition is not asso- 
ciated with fever. 

Actinomycosis attacks one quarter, but may extend to 
other quarters. The enlargement is not great and develops 
slowly. The corresponding lymph-gland is usually not 
enlarged ( only in very old udder-actinomycosis is there any 
great enlargement). 

The milk is normal in appearance for more than a 
month, but finally becomes yellow and purulent. It is then 
a yellow, serous, thin fluid pus containing flakes of pus. 
Milk-gangrene is exceptionally rare. Secondary infections 
and abscess formation are rare and the condition is not 
accompanied by fever. 

Typical udder-infections which present no distinct swell- 
ing of the udder are caused by streptococci. 

Typical chronic streptomycosis is a milk-infection 
[parenchymatous mastitis]. It usually affects one quarter, 
but may spread to the other quarters by infection. 

The milk is changed gradually. It becomes yellow, 
thick as cream, and finally almost pulp-like in consistency, 
and contains a great number of floating pus-cells. Milk- 
gangrene is exceptionally rare. 



CLINICAL DL^GNOSIS OF MASTITIS 125 

Ultimately the udder becomes altered. It does not 
collapse after milking, especially the parts around the base 
of the teats, and is firm or hard, but not distinctly enlarged. 
These changes slowly extend laterally and upward. The 
supramammary lymph-glands are not affected. Secondary 
infections are rare. Abscesses do not occur. The condition 

is free from fever. 

Microscopic Examination of Udder-infections.— 
This corroborates or corrects the clinical diagnosis. 

The material to be examined is the wound secretion 
in wound-infections and the sediment of the milk in genuine 
udder-infections. In these examinations one may expect 
to find great numbers of pyogenes bacilli in the pathologic 
products. Conversely the tubercle bacilli and actinomyces 
colonies are only present in small numbers. 

In acute milk-infections [parenchymatous mastitis] 
great numbers of bacteria are present during the first few 
days, but later become few. In typical chronic streptomy- 
cosis the bacteria are very numerous. 

In cases where the cocci appear in the diplococcus form 
in coccus infections a diagnosis of staphylomycosis or strep- 
tomycosis may be very difficult. 

A uniformly round shape and many single cocci point 
toward staphylococci, while an oval shape and the absence 
of single cocci emphasize streptococci. If in the first case 
the cocci are grouped in grape-like bunches and in the last 
case in chains, and capsules are present, the diagnosis is 
certain. 

Summary 

1. Mastitis caused by external force. 

Udder-bruises and udder-wounds. 

2. Udder-infections. 

A. Macroscopic diagnosis. 



126 MASTITIS OF THE COW 

1. Infected udder-wounds. 

a. Acute wound-infection. 

Streptomycosis. 

Staphylomycosis. 

Colibacillosis. 
6. Chronic wound-infection. 

Pyobacillosis. 

Tuberculosis. 

Actinomycosis. 

2. Genuine udder-infections. 

a. Acute genuine udder-infections. 

Acute streptomycosis, staphylomycosis, and 
colibacillosis. 

b. Chronic genuine udder-infections : 

aa. At^^pical chronic udder-infections : 

Atypical chronic streptomycosis (which, 
together with pyobacillosis and tu- 
berculosis, complicates acute infec- 
tions). 

bb. Typical chronic udder-infections. 

1. With distinct udder swelling. 

Pyobacillosis. 
Tuberculosis. 
Actinomycosis. 

2. Without distinct udder swelling. 

Typical chronic streptomycosis. 
B. Microscopic diagnosis. 

Material for examination. 

Quantity of bacteria in pyobacillosis, tuberculosis and 
actinomycosis, in acute milk-infections and in typical 
chronic streptomycosis. 
Differential diagnosis between streptococci and staphy- 
lococci. 
Streptomycosis is the most variable of all the genuine udder- 
infections since it can have at least three different clinical forms. 

In general a careful examination of the animal, together with a 
good anamnesis, can enable one to arrive at a comparatively cor- 
rect diagnosis. 

The length of the course corrects or corroborates our diagnosis. 



CHAPTER XIV 

AUTOPSY 
Post-mortem Technic 

The udder, together with the supramammary lymph- 
glands, is dissected from the abdominal wall and divided into 
its two lateral halves with a knife. 

The halves are placed in a certain definite position on a 
table or other suitable surface in order to facilitate observa- 
tion of the teats and lesions and remembrance of their 
topography. Each half is placed upon its median surface, 

bringing the lateral or exter- -Q p ■ ^ 

nal side uppermost, teats « y y >1 J 

proximal of the autopsist ^j^— .^ tT^ 

and abdominal margin distal, fio. 29— Position of halves of the udder 

, « , at autopsy, t. = left. H. — right 

Thus the fore quarter of the 

left half is at the left and the fore quarter of the right half 

is naturally at the right (Fig. 29). 

External Examination. — The normal udder-half 
lies limp, collapsed and flattened out upon the table. The 
half is somewhat thin and its inferior margin fairly sharp. 
The consistency of the udder is soft and elastic. 

One looks for wounds and other lesions and observes 
their position, size, number, consistency, degree and dis- 
tribution. If milk is present a little should be milked into 
the hand from each quarter. If the milk from any quarter 
is altered a sample should be collected from each diseased 
quarter. 

Lymph-glands. — These are examined in situ. Their 
size under physiological conditions is not constant, though 
the diameter is usually 6 to 9 cm. Their size is commonly 
indicated by the terms very greatly, moderately, shghtly 
or not at all enlarged. 

127 



128 MASTITIS OF THE COW 

The lymph-glands are then divided by a longitudinal 
incision, the halves laid apart and the structure examined 
for lesions. One should carefully observe whether the in- 
cision be dry. Normally it is moderately dry. When juicy 
it indicates oedema. It may be hard from induration. If 
any of these conditions be present transverse incisions are 
made through them. 

If a teat is affected it should be amputated close to its 
base and the cistern and teat canal examined after its 
ablation. 

Cut Surface of the Udder. — Each udder-half is now 
laid open like a book by making a sagittal longitudinal 
incision parallel to the table and extending to the cisterns. 

Under physiological conditions the incision is more or 
less juicy and the juice in the incision consists of milk. The 
cut surface bulges outward so that it is slightly convex. 
It presents a fine net-like framework of white connective 
tissue which divides the structure into an inestimable num- 
ber of closely associated flaccid rounded parts ranging in 
size from a lentil to a pea, called lobuli. Within the lobuli 
one can see the milk- filled tubuli as exceptionally small, just 
barely visible white points called milk points. During the 
lactation period the lobuli are grayish-white and during the 
quiescent period they are often yellow. The consistency 
is soft, elastic, tough, and it resists tearing or crushing. 
More or less milk is found in the cisterns and milk canals, 
and their mucous membranes are white and uniform. 

Under pathological conditions the cut surface may pre- 
sent many different alterations. The juice in the incision 
may consist of pus or other pathological products. If the 
cut surface is even, not convex, it points toward diminished 
elasticity following sclerosis or other changes. If the con- 
sistency of the cut surface is firm but pliable, it indicates 
engorgement and distension of the elastic gland vesicles 
with firm contents, such as fibrin or cells. In the same 



AUTOPSY 129 

manner the consistency may be soft and elastic, like India 
rubber, when the vesicles are filled with water. If they are 
filled with firmer substances as of pulpy consistency the cut 
surface will be firm but friable. Upon application of 
pressure to the diseased lobuli pus may be expressed from 
the incised collecting ducts. If the milk points have dis- 
appeared from a number of lobuli in a lactiferous udder it 
indicates a diminution or suppression of milk secretion, 
thus diminution of the volume or destruction of the tubuli. 
One may find abnormal contents such as blood or pus in 
the cisterns and milk-ducts. 

If the condition is extensive, radiating, transverse in- 
cisions are made through the lesions down to the inferior 
side. 

Post-mortem Diagnosis 

Upon external examination one may possibly observe 
the presence of wounds or other perceptible lesions, such as 
induration. 

UDDER-WOUNDS 

Infected wounds are important on post-mortem exam- 
ination. 

The Post-mortem Diagnosis. — Infected wounds are 
easily determined. The rule is that all open and moistened 
wounds are infected. If it contains a yellow or grayish- 
red or more or less thick pathologic fluid it may positively 
be designated an infection. If the secretion stinks, gan- 
grene has complicated the infection. 

A deep incision is made through the wound, so that the 
surfaces may be separated and properly examined with the 
eye. ( This incision is usually a transverse incision through 
the udder.) 

If the walls of the wou/nd are red an acute infection is 
indicated. This may be a simple streptomycosis, staphylo- 

9 



130 MASTITIS OF THE COW 

mycosis or colibacillosis or a mixed infection which is more 
common. This can be determined with the microscope. 

The wound secretion can be serous and red or grayish- 
red or thick fluid yellow pus. The walls of the wound are 
firm and more or less thick. The inner side is smooth, 
uneven or warty. 

If the walls of the wound are not red, but white, or green 
from gangrene, a chronic infection is indicated. It may be 
pyobacillosis, tuberculosis or actinomycosis. 

These wounds present the same appearance as described 
in the previous chapter on clinical diagnosis. In addition 
one sees the specific lesions of these diseases in the cut sur- 
face, walls of the wound and in the adjacent tissue. 

SOLIDIFICATION OF THE UDDER 

These lesions can be produced by bruises or by infection. 

An intense red coloring of the cut surface is indicative 
of a fresh bruise or an acute infection. 

Fresh Udder Bruises. — The udder shows a hard cir- 
cumscribed swelling. The incision is juicy, and the juice 
of the incision consists of unaltered milk or milk partly 
mixed with blood. The cut surface likewise presents a cir- 
cumscribed altered area which is even, firm but friable. 
It is red in color, but shows a distinct outline. A few lobuli 
are red, due to blood infiltration following hemorrhage, 
others are yellowish-gray and show no milk points. The 
cisterns and milk-ducts contain unaltered milk or milk 
mixed with blood. 

Acute Udder-infections. — These concern the milk- 
infections : parench\Tnatous mastitis, acute streptomycosis, 
staphylomycosis and colibacillosis. 

The quarter is more or less swollen and firm. The 
incision is juicy, and the juice consists of yellow pus. The 
entire cut surface or only its inferior portion is even but 



AUTOPSY 131 

friable. The color is grayish-red, due to infiltration with 
blood. Here and there one may see circumscribed dark 
red areas due to hemorrhage, or circumscribed yellow, firm 
or pulpy areas of necrosis. The lesion is distinct and no 
decomposition of the blood is present. The milk points are 
absent. Yellow pus or yellow fibrin cylinders are ex- 
pressed upon apphcation of pressure to the lobuli. Yellow 
pus or yellow firm masses of fibrin are found in the cisterns 
and in the milk-ducts. 

Complication with gangrene is easily determined by the 

odor. 

A macroscopic differential diagnosis of these conditions 
is usually impossible, although firm, croupous membranes 
point toward streptomycosis and a decided purulent soften- 
ing of croupous membranes toward staphylomycosis. 

Staphylomycosis can be very severe and fatal, however, 
in which case the udder shows diffuse necrosis (severe pri- 
mary lesion) without inflanmiation. This post-mortem 
picture is different and very characteristic. 

The affected quarter is distinctly swollen and hard. The 
incision is juicy and the cut surface presents a red serous 
fluid. The cut surface is even and its consistency is firm 
but friable. Here and there it shows black and red circum- 
scribed areas due to blood infiltration and hemorrhage. The 
cut surface is red and rich in blood for the most part. This 
lesion is very distinct in consequence of a uniform distribu- 
tion of the red coloring matter, which is not confined to the 
injected blood-vessel or the areas infiltrated with blood, but 
also uniformly stains the connective tissues, parenchyma, 
mucous membranes and secretions. [Imbibition of liber- 
ated haemoglobin following decomposition of red blood 
cells.] The milk points in the lobuli are entirely absent. 
Pressure upon the lobuli causes a red fluid to be expressed. 
Twig-like cylindrical red-stained masses of fibrin can be 



132 MASTITIS OF THE COW 

removed from the cisterns and milk-ducts. Gangrene, 
which is a conmion complication, produces a stinking odor 
in the udder. 

The acute infections, as secondary infections, may in- 
vade the chronic udder-infections, yet these are usually easy 
to recognize by their particular post-mortem characteristics 
(see later). 

A cut surface, hut slightly or not at all red-stained, 
indicates ( 1 ) a chronic infection or ( 2 ) the healing process 
of a bruise or of an acute infection. 

The chronic infections manifest their individual charac- 
teristic post-mortem picture. From the autopsy point of 
view they may be divided into typical stroma-infections and 
typical milk-infections. 

The typical stroma-infections are pyobacillosis, tuber- 
culosis and actinomycosis. They are usually easy to recog- 
nize. If the condition is very early the diagnosis may be 
difficult and the microscope must be used. 

Pyobacillosis. — The affected quarter is hard and mod- 
erately swollen. The lymph-glands are not changed. 

Upon incising the lesion, the knife is smeared by a yel- 
lowish-green, thick, caseous mass of salve-like consistency. 
The cut surface is even and yellowish-gray. Its consis- 
tency is firm. Here and there one observes variable-sized 
cavities containing yellowish-green, caseous masses, which 
are surrounded by thick connective-tissue walls, the in- 
ternal side of which are smooth. The yellowish-gray lobuli 
show no milk points, but not infrequently a few or more 
small yellow, sharply defined necrotic or caseous points. 
Pressure upon the lobuli causes yellow, caseous cylinders 
to be expressed. Numerous milk canals are distended with 
these yellowish-green caseous masses. Their walls have 
become thick, white connective-tissue structures trans- 
formed into fistula?. In other milk canals and in the cis- 
terns one may observe spongy croupous membranes. The 



AUTOPSY 133 

mucous membranes in the cisterns may show small, red, 
pointed gi'owths (condyloma). In the common complica- 
tion of gangrene a stinking odor is present. 

Tuberculosis. — The affected quarter is usually hard 
and severely swollen. 

The corresponding lymph-gland is increased in size. 
The incision in the lymph-gland is either succulent, as in 
udder-tuberculosis, or more or less dry and often gritty, as 
in advanced udder-tuberculosis. The juicy cut surface is 
spongj^ in consistency and shows few, if any, small caseous 
foci. The dry cut surface is caseous for the most part and 
therefore yellow in color. The consistency is firm and in 
calcification very firm. 

The incision in the udder is comparatively dry and in 
advanced tuberculosis gritty, due to calcification. The 
affected inferior portion of the cut surface is even, the con- 
sistency is firm and the color grayish-yellow. The superior 
portion of the cut surface bulges or is convex. It shows 
a number of yellowish-gimy, round, protruding nodules, 
varying in size from a poppy seed to a hemp seed, or small 
wart-like structures situated here and there in the lobuli. 
The lobuli present no milk points, but small yellowish-white 
caseous points instead. Usually, but not invariably, yellow 
caseous masses may be expressed by pressure upon the 
lobuli. In addition, if the condition is old, one may see 
yellow, round, sharply circumscribed necrotic foci of vari- 
able size ranging from a hemp seed to a walnut or larger. 
The necrotic parts are loose and thickly fluid or firmly 
caseous. It can be calcareous and the calcification begins 
in the centre and is manifested by a brighter point or nucleus 
which later enlarges. The necrotic area is usually sur- 
rounded by very thin connective tissue. In the superior 
convex part of the cut surface the color is whitish-gray. 
The consistencv is very soft and elastic. The lobuli are 



134 MASTITIS OF THE COW 

increased in size and the milk points very prominent, due 
to milk stasis. 

In the cisterns and milk ducts one can observe faintly 
yellowish colored milk, or in advanced tuberculosis yellow- 
ish croupous membranes. Here the mucous membrane 
may also present small, round, crateriform tuberculous 
wounds. In simple or uncomplicated tuberculosis, gan- 
grene never occurs. 

Actinomycosis. — The affected quarter is hard and 
usually enlarged to a lesser degree. The corresponding 
lymph-gland is usually not involved. Only in very old 
udder-actinomycosis is it enlarged, when on section it pre- 
sents grayish-yellow, protruding, round, soft, actinomy- 
cotic foci. 

The incision in the udder is somewhat dry. The cut 
surface is even in the affected inferior portion. Here and 
there one may see sharply defined, round, distinctly pro- 
truding or convex yellowish-gray, soft, elastic foci ranging 
in size from a poppy seed to a hemp seed and larger. Within 
these foci one finds a number of smaller, yellowish-white, 
white to brown granules or actinomyces colonies, which are 
hard and sharp to the touch, due to calcification, if the con- 
dition is old. The surrounding parts are grayish-white, 
without milk points and of tendon-like consistency due to 
sclerosis. 

In the milk canals and cisterns one finds wounds from 
the walls of which grow yellowish-gray, round, tumor-like 
spuds of granulation tissue from the size of a pea to that of 
a bean, which contain yellowish-brown actinomyces gran- 
ules. Simple actinomycosis shows no tendency toward 
gangrene. 

The chronic milk-infections are only streptomycosis. 
From the post-mortem point of view as well as the clinical 
standpoint these chronic streptomycoses may be divided into 



AUTOPSY 135 

atypical chronic and typical chronic streptomycosis. These 
forms, however, are not sharply separated, but present 
transition forms. 

Atypical Chronic Streptomycosis. — The affected 
quarters are usually moderately swollen and hard. The 
lymph-gland is not involved. The incision is dry. The 
cut surface is even and uniform. The color is grayish- 
white and the consistency is tendinous and sclerotic. 

The lobuli present no milk points. They are whitish- 
gray due to sclerosis or yellowish-gray from inflammation. 
Fibrin plugs are expressed by pressure upon the yellowish- 
gray lobuli. There are yellow, firm and tough croupous 
membranes in the milk-ducts and cisterns. At the same 
time one may observe grayish-white, somewhat firm ne- 
crotic sequesters in the cut surface which are the size of a 
pigeon's egg or larger, show an irregular external surface 
and contain signs of udder-tissue. As a rule the sequester 
is moistened with a small quantity of yellowish pus and sur- 
rounded by a thick white connective-tissue wall. 

Typical Chronic Streptomycosis. — The affected 
quarter is not enlarged, but frequently diminished in size, 
yet the quarter is not collapsed and thin, and it is somewhat 
thicker, especially at the base of the teats, but the volume 
is diminished, however. The consistency is somewhat firm. 

The incision is juicy and the juice consists of yellow, 
thick, cream-like milk mixed with pus. The cut surface is 
even, wliitish-gray and tendinously firm, at least in the 
inferior parts around the base of the teats. A little above, 
the cut surface is yellowish-gray, firm and somewhat friable, 
due to inflammation. The altered lobuli present no milk 
points, but thick, yellow, cream-like milk can be expressed 
from them by applying pressure. The superior part of the 
cut surface presents unaltered lobuli which show milk 
points. The milk-ducts and cisterns contain yellow, thick, 
cream-like milk. 



136 MASTITIS OF THE COW 

Udder-hruises and acute infections in the state of heal- 
ing may be mistaken for chronic streptomycosis. The fol- 
lowing characteristics are important for a differential 
diagnosis : 

Udder-bruises in State of Heajling. — The udder 
presents a nicely circumscribed hard swelling. The cut 
surface in this part is even, whitish-gray and of tendinous 
consistency. In the other portions both the udder and the 
milk are unchanged. 

The Acute Infections in the State of Healing. — 
The udder is somewhat swollen and hard. The incision is 
succulent, and the juice consists of a mixture of unaltered 
milk and yellow pus. The cut surface is usually convex 
and the consistency somewhat soft and elastic. Here and 
there among the noniial lobuli there are groups of yellowish- 
gray non-protruding lobuli without milk points, which are 
of firm but friable consistency. With pressure applied to 
these altered lobuli pus is expressed. 

Summary 

1. Post-mortem technic. 

Ablation of the udder. 

Position for examination. 

External examination. 

Lymph-gland. 

Teats. 

Cut surface of the udder. 

2. Post-mortem diagnosis. 

A. Infected wounds. 

1. The walls of the wound when red colored, streptomycosis, 

staphylomycosis, colibacillosis. 

2. The walls of the wound when not red colored, pyobacil- 

losis, tuberculosis, actinomycosis. 

B. Solidification of the udder. 



AUTOPSY 137 

1. Severe redness of cut surface. 
a. Fresh udder-bruises. 

h. Acute udder-infections. 
aa. Inflammation. 

Acute streptomycosis, staphylomycosis, colibacil- 
losis. 
bb. Primary lesion, diffuse udder-necrosis. 
Staphylomycosis. 

Possibility of the acute infections being com- 
plications of the chronic infections. 

2, Cut surfaces which are faintly or not at all red. 
a. Chronic infections. 

aa. Typical stroma-infections. 

Pyobacillosis. 

Tuberculosis. 

Actinomycosis. 
hb. Typical milk-infections. 

Atypical chronic streptomycosis. 

Typical chronic streptomycosis. 
h. Bruises and acute infections in healing stages. 
aa. Bruises in state of healing. 
5b. Acute infections in healing. 



CHAPTER XV 

IMPORTANCE OF MASTITIS TO MILK CONTROL 

If the milk is to be used as food for man it must have a 
normal appearance and must contain no bacteria which are 
pathogenic for the human family. If the milk is mixed 
with blood, due to bruising of the udder, it is unfit for use 
as a human food. Naturally, however, the milk from the 
healthy quarters may be utilized. 

The udder-infectioTis are more important. Streptococci, 
staphylococci, colon bacilh, tubercle bacilli and actino- 
myces fungus cause disease in man. Of the infectious 
organisms of the udder of the cow the pyogenes bacillus 
alone is not concerned in the production of disease in man 
so far as is known. Caution demands, however, that it be 
considered dangerous to the human family until the con- 
trary has been proved. 

The Following Rules are Indicated. — All milk 
from the infected quarter is unfit for use as food for man. 

Even if the other quarters of the udder are free from 
the infection, the milk from the infected quarter can easily 
get into the milk from the healthy quarters during milking 
in spite of every precaution. Therefore the milk from the 
healthy quarters should be pasteurized or boiled before it is 
used, as a precautionary measure. 

To prevent contamination of the milk of the other cows 
the diseased animal must be isolated and milked last. For 
the same reason the milk from the diseased quarter must 
be disinfected so as to avoid unnecessary increase in the 
pathogenic bacterial flora of the cow stable. 

When the infection disappears and the milk becomes 
normal again it may be used without boiling or pasteurizing 
and the rules concerning isolation may be discarded. 

138 



IMPORTANCE TO MILK CONTROL 139 

In acute udder-infections where the changes in the milk 
occur simultaneously with those in the udder, these rules 
are easy to follow. These infections may be recognized by 
the attendants without the assistance of a veterinarian. 

The udder is considered healthy when it is no longer 
swollen and hard, and when the milk of a sample milking 
presents a completely normal appearance and contains no 
fibrin or pus flakes. This test is carried out by the 
veterinarian. 

In typical chronic infections the above rules are difficult 
to observe, since the milk in these infections retains its nor- 
mal appearance weeks or months after the infection has 
taken place. The acute infections can be recognized by 
the attendants while, on the contrary, the typical chronic 
cases can only be diagnosed by the veterinarian. 

If a milk-test record is kept, one can take note of all 
cows which show a premature and rapid diminution in milk 
secretion and then examine their udders and in this way, 
perhaps, make a timely diagnosis. If no milk record is 
kept one is compelled to examine all the udders. 

The examination is best made after milking, when the 
udders are relaxed and collapsed. In this condition a swell- 
ing or thickening is more easily determined. The udder is 
inspected from behind and from both sides. If lesions are 
observed in this way a closer examination of the udder is 
made. The lesion is palpated, as are the lymph-glands, 
and if a chronic condition is suspected in the udder examina- 
tion of a milk sample is ordered. 

The milk sample should only be taken from the dis- 
eased quarter. A microscopic examination of the sediment 
of the milk sample confirms or contradicts the tentative 
diagnosis. 

If a chronic udder-infection is diagnosed one is gov- 
erned by the rules designated, except in udder-tuberculosis, 
in which condition the animal must be slaughtered as unfit 



140 MASTITIS OF THE COW 

for use as a milch cow, according to our [Sweden] statu- 
tory regulations. [No Federal law in this country compels 
an owner to kill such an animal. Law prevents interstate 
shipment. Most municipal laws prevent sale of milk from 
such a cow in the municipality.] 

If the examination establishes no definite diagnosis or 
does not dispel the suspicion of a chronic infection, one may 
proceed as before stated on the history of the animal until 
an examination, eight to fourteen days later, confirms the 
diagnosis or completely removes all suspicion of the case. 

Such an examination must be undertaken at least once a 
month in order to constitute an effective milk control. To 
establish a certainty that none of the milch cows have udder- 
tuberculosis these examinations must be repeated every 
fourteen days. 

If the milk is to be used as food for calves or pigs one 
should follow the same general principles. 

These animals may be fed the milk from cases of chronic 
mastitis, if it is of normal appearance and providing it is 
boiled before being used. 

Summary 

1. Milk as food for man. 

A. Bloody milk. 

B. Milk containing infectious organisms. 

1. Rules: 

a. Milk from an udder-infection is unfit for use 

by man. 

b. Milk from the other quarters can be used 

when boiled. 

c. The diseased cow is isolated and milked last. 

d. The infected milk is disinfected. 

e. The rules are cancelled when the infection dis- 

appears. 



IMPORTANCE TO MILK CONTROL 141 

2. Application of rules : 

a. Acute infections. 

Diagnosis. 

Test to determine disappearance of infection. 

b. Typical chronic infections. 

Diagnosis. 

Slaughter of animals. 
Suspected chronic infections. 
Time between examinations. 
2. Milk as food for animals. 

The chronic udder-infections have a great economic significance 
in regulating milk control. The animals may produce a consider- 
able quantity of milk which can be of normal appearance, while at 
the same time this milk cannot be used as food for man. 

These infections are very common as may be seen by the fol- 
lowing figures compiled at an abattoir: In the year 1905 there 
were inspected in the abattoir at Malmo 6936 cows, of which 
1042, or 15 per cent, were shown to be affected with mastitis 
(annual report of the Malmo Abattoir for 1905, edited by A. M. 
Bergman, director). 

These cases of mastitis or udder-infection in abattoirs are 
nearly always chronic. The acute infections are seldom seen 
during the quiescent state of the udder, and cows are only slaugh- 
tered in the lactation period when circumstances demand imme- 
diate slaughter, which is very rare with acute udder-infections in 
abattoirs. 

These cases of mastitis, or better, the chronic udder-infections 
in the abattoirs, are chronic streptomycosis or pyobacillosis. 
Udder-tuberculosis or udder-actinomycosis is usually listed in the 
abattoir records under the head of tuberculosis and actinomycosis, 
not as mastitis. In the report referred to above the cases of 
udder-tuberculosis were computed with the figures on mastitis. 

Fifteen per cent, of the cows had been affected with chronic 
udder-infections. 

The same report in 1905 showed 155 cases of udder-tubercu- 
losis, which is ca. 2.2 per cent, of the number of cows slaughtered. 

Figures from the journal of the Veterinary High School for 



142 MASTITIS OF THE COW 

examination of udder-tuberculosis show us the occurrence of 
chronic udder-streptomycosis, udder-pyobacillosis and udder- 
actinomycosis. 

In 1905 and 1906 there were observed: 

Streptococci in 192 milk samples 

Pyogenes bacilli in 56 milk samples 

Actinomyces fungus in 10 milk samples 

Total 258 milk samples 

Taking these figures as a standard the above-mentioned cows 
had: 

ca. 9.5 per cent. Chronic udder-streptomycosis. 
ca. 2.8 per cent. Udder-pyobacillosis. 
ca. 0.5 per cent. Udder-actinomycosis. 

Total, 12.8 per cent. 

If the percentage of udder-tuberculosis be added we have the 
following figures: The 6936 cows slaughtered in Malmo in 1905 
showed : 

ca. 9.5 per cent. Chronic udder-streptomycosis. 

ca. 2.8 per cent. Udder-pyobacillosis. 

ca. 2.2 per cent. Udder-tuberculosis. 

ca. 0.5 per cent. Udder-actinomycosis. 

Total, 15 per cent. Chronic udder-infections. 

These figures suggest how common such udder-infections are. 
One should assume that these figures apply to every standard of 
cow, but should consider that the statistics were compiled in an 
abattoir and that they only include animals slaughtered for vari- 
ous reasons such as old age and disease. 

According to the estimate of a practical farmer ca. 16 per 
cent, of the cows must be slaughtered yearly under ordinary cir- 
cumstances. 

The 6936 slaughtered animals mentioned, according to these 
figures, would indicate a total of 43,350 cows. 



IMPORTANCE TO MILK CONTROL 143 

The individual percentage would show the following figures. 
Of the total number of cows there are annually diseased : 

ca. 1.52 per cent, with Chronic udder-streptomycosis. 

ca. 0.45 per cent, with Udder-pyobacillosis. 

ca. 0.35 per cent, with Udder-tuberculosis, 

ca, 0.08 per cent, with Udder-actinomycosis. 



ca. 2.40 per cent, of the total number of cows showing udder- 
infections. 

Out of 200 cows one may expect five cases of chronic udder- 
infection yearly, and of these three are usually streptomycosis and 
the remaining two may be one of the three other chronic udder- 
infections. Of these pyobacillosis is the most common and occurs 
in ca. 1 case in 200 cows ; next comes tuberculosis, ca. 1 case in 
300 cows, and finally actinomycosis, the least frequent, with ca. 1 
case in 1200 cows computed on a yearly basis. Naturally the 
figures are not so uniform. 

The first two figures are fairly constant but the last two are 
not. 

The figures on tuberculosis were taken from our most heavily 
infected tuberculous districts and are therefore not a fair average 
for the presence of tuberculosis in the entire country. The figures 
for the whole country are decidedly lower. In certain parts of 
Sweden, as in the north, udder-tuberculosis is very rare. Naturally 
it is not present at all in the districts which are free from reactions. 

The figures on actinomycosis taken from the journals of the 
Veterinary High School of material from the different regions of 
Sweden are perhaps a fair average for the occurrence of this dis- 
ease in the country. Actinomycosis, however, is not uniformly dis- 
tributed in the country. There are regions where udder actinomy- 
cosis occurs with relative frequency and others where it is not 
present at all. 



CHAPTER XVI 

THE IMPORTANCE OF MASTITIS TO MEAT 
INSPECTION 

Examination 

The udder should be examined with an eye for swell- 
ings and palpated for thickenings. 

When such lesions are observed the half of the udder 
affected, together with the other half, is laid open by a 
sagittal longitudinal incision extending through the teats. 
The appearance of the cut surface facilitates a quick de- 
termination of the nature and extent of the condition. 
When the udder has been thoroughly examined the supra- 
mammary lymph-glands are inspected. If one or both of 
these glands are swollen and cedematous one may logically 
suspect udder-tuberculosis. If this suspicion is not proved 
to be absolutely unfounded the meat in these cases is judged 
as though udder-tuberculosis had been diagnosed. When 
tuberculous foci are present the diagnosis is positive. ( I have 
seen one case of extensive tuberculosis of the supra-mam- 
mary lymph-glands, however, without any visible tuber- 
culosis in the corresponding udder. This was a case of 
wound infection, as a tuberculous wound was found in the 
gland.) The less frequent actinomycotic foci must not be 
confused with tuberculosis. 

Judgment 
Udder. — That half of the udder found to be diseased, 
together with its corresponding lymph-gland, is unfit for 
use by man. [The entire udder is condemned.] If a 
decided sclerosis of an injury is present and no pus can be 
expressed it may be passed. [Entire udder is condemned.] 

144 



IMPORTANCE TO MEAT INSPECTION 145 

If one half of the udder is condemned because of an 
udder-infection the other half must be critically inspected. 
It may only be passed when it is manifestly free from 
pathological lesions and when the udder-infection found in 
the first half is plainly of a local character (see later). 
[Entire udder is condemned.] 

Meat. — Only the infectious inflammations of the udder 
can render the meat unfit for man. 

Acute udder-infections are usually local in character. 
They are milk-infections and wound-infections. The 
former are the most important and the location of the 
organisms is in the tubuli, as is the case in the more virulent 
staphylomycosis with diffuse necrosis of the udder. 

Infection of the blood or bacteraemia rarely occurs. It 
may be recognized by swelling of the spleen, haemolysis, or 
by acute embolic pneumonia. A microscopic examination 
of the spleen or blood must determine the judgment of the 
meat. If Gram negative rod-shaped bacteria or Gram 
positive cocci are found the meat is condemned. [Micro- 
scopic examination is not necessary. Carcass is condemned 
on gross lesions of bacteraemia.] 

An udder-colibacillosis may cause infection of the meat. 
This infection is especially difficult to determine. If an 
acute udder-infection is established and if the cut surface 
of the udder is severely reddened, a microscopic examina- 
tion of the juice from the incision in the udder must 
determine whether or not the meat is fit for food. If a 
considerable number of fairly large, short and clumpy Gram 
negative bacilli with rounded ends are found the meat is 
declared unfit for use by man. [If local the entire udder 
is condemned. If acute diffused mastitis the entire carcass 
is condemned. B. A. I. Order 150, Regulation 13, Section 
18, d.] 

If an acute udder-infection is complicated with gan- 
grene the meat may only be used after we have proved that 

10 



146 MASTITIS OF THE COW 

it bears no abnormal odor. [The carcass should be care- 
fully examined for lesions of septicemia.] 

Chronic Udder-infections. — Their type plays a great 
part in the judgment of meat. 

Chronic udder-streptomycosis is always of a local char- 
acter. The auriculo-ventricular valves of the heart may 
show an endocarditis which might be the cause. Should 
such really be the cause the meat may be used only after a 
careful inspection and excision of metastatic lesions in the 
meat. The heart, together with the organs containing 
metastatic processes must be condemned. [Entire carcass 
condemned.] 

If gangrene complicates the udder condition the meat 
must be proved free from odor before it may be used. 
[Entire carcass condemned.] 

Pyobacillosis and actinomycosis of the udder are usually 
local conditions. They may be generalized, however, the gen- 
eralization manifesting itself usually in the internal organs 
only, as the lungs and liver. Condemnation of meat, fol- 
lowing generalization of these conditions, is not, as a rule, 
demanded. In complications of pyobacillosis with gan- 
grene the odor of the meat determines the judgment. 
[Entire carcass condemned.] 

Udder-tuberculosis, as a rule, is an indication of gen- 
eralized tuberculosis. Udder-tuberculosis is local and pri- 
mary only when the lungs are free from the disease. 

In many cases of generalized tuberculosis only the in- 
ternal organs are involved, leaving the muscles and bones 
unaffected, so that all or part of the meat may safely be 
used. [Entire carcass condemned.] According to the sta- 
tistics of the abattoir at Malmo for the year 1905, edited 
by Director A. M. Bergman, 155 cows were affected with 
udder-tuberculosis of which, in 29 cases, or 19 per cent., the 
tuberculosis was of slight extent, so that only single parts 
had to be condemned. 



IMPORTANCE TO MEAT INSPECTION 147 

In generalized tuberculosis, therefore, one carefully in- 
spects the body, incises the body lymph-glands and ex- 
amines the vertebrse and sternum after longitudinal 

division. 

If the udder-tuberculosis is local or the tuberculosis is 
generalized, but the skeleton and muscles unaffected, and 
the meat healthy in other respects, the meat can be passed 
for use. [Entire carcass condemned.] 

One should not forget to carefully determine whether 
or not the supramammary and lumbar lymph-glands are 
swollen. 

Summary 

1. Inspection: 

A. Udder. 

B. Suprammary lymph-glands. 

2. Judgment: 

A. Udder. 

1. The diseased half of the udder. 

2. The other half of the udder. 

B. Meat. 

1. Acute udder-infections. 

Bacterasmia. 

Colibacillosis. 

Gangrene. 

2. Chronic udder-infections. 

a. Chronic udder-streptomycosis. 

Endocarditis. 

Gangrene. 
h. Udder-pyobacillosis and actinomycosis. 

Generalization. 

Gangrene in pyobacillosis. 
c. Udder-tuberculosis, 

Lopal udder-tuberculosis. 

Generalized tuberculosis. 

Lymph-glands. 



CHAPTER XVII 

POST-MORTEM REPORT 
I. Single Infections 

A. STREPTOMYCOSIS 

1. Atypical chronic streptomycosis in both posterior 
quarters of the udder. 

Both posterior quarters were swollen and firm in con- 
sistency. Both quarters presented the same lesions. The 
incision was very dry. The entire lower portion of the cut 
surface was even, grayish-yellow and very firm. The lobuli 
in this region were small and without milk points. Yellow 
cylinders of fibrin were expressed, and the milk-ducts and 
cylinders were filled with yellow fibrin. The other areas 
of the udder showed no lesions. 

In the fibrin a few small lancet-shaped Gram positive 
cocci, arranged as diplococci, were observed (streptococci). 

2. Atypical chronic streptomycosis of the left posterior 
quarter with nodular necrosis. 

Only the left half of the udder was autopsied. 

The left posterior quarter was moderately swollen and 
firm in consistency. 

The incision in the quarter was somewhat dry. The 
cut surface was even, yellowish-gray and very firm. The 
lobuli in this region were very small and showed no milk 
points. Yellow cylinders of fibrin were expressed. Whitish- 
gray, round, convex, unaltered lobuli showing distinct milk 
points were distributed here and there. In the posterior 
inferior part there was a round cavity the size of a hen's 
egg surrounded by a white, thick connective-tissue wall. 
It contained yellowish-gray pus and also a grayish-yellow, 

148 



POST-MORTEM REPORT 149 

firm, necrotic body of irregularly rounded shape and with 
uneven, ragged external surface. The body was of firm 
but friable consistency. In the cisterns and the milk-ducts 
yellow fibrin and viscid croupous membranes were observed. 
Other parts of the udder manifested no alterations. 

A great number of small Gram positive cocci grouped 
in twos or short chains, for instance, streptococci, were 
observed in the fibrin and the necrotic tissue. The diag- 
nosis was corroborated by cultures. 

3. Atypical chronic strcptomycosis in the right anterior 
qtmrter, together with a typical chronic strcptomycosis in 
both posterior quarters. 

The right anterior quarter of the udder was slightly 
changed, disproportionate and hard. Both posterior quar- 
ters were decreased in size, but still thick and somewhat 
firm. 

Right anterior quarter : The incision was somewhat dry. 
The cut surface was even, grayish-white and firm. The 
lobuli were small and presented no milk points. Yellow 
fibrin cylinders were expressed. Groups of grayish-white, 
convex, soft and elastic unaltered lobuli showing milk 
points were present here and there. Firm yellow fibrin 
was observed in the milk-ducts and the cisterns. 

Both posterior quarters presented the same lesions. 
The incision was succulent and the liquid of the incision 
consisted of a yellow, cream-like pus. The cut surface 
was even, grayish-white and tendinous. The lobuli were 
small and presented no milk points. Yellow cream-like 
pus was found in the milk-ducts and the cisterns. No lesions 
were found in the other parts of the udder. 

In the fibrin of the right anterior quarter a great number 
of Gram positive cocci arranged in twos or short chains were 
present ( streptococci ) . 

In the pus of both posterior quarters a great number 



150 MASTITIS OF THE COW 

of Gram positive cocci in long chains were found (strep- 
tococci). 

B. STAPHYLOMYCOSIS 

1. Staphylomycosis of the right half of the udder as well 
as the left anterior quarter. Diffuse necrosis of the udder. 

The cow had to be slaughtered. 

The right half of the udder as well as the left anterior 
quarter were greatly swollen and hard. 

The lymph-glands were slightly swollen. The incision 
was succulent with lymph and the cut surface was gray, 
moist and friable (oedema). The diseased parts of the 
udder presented the same lesions. The incision was juicy 
with a dark red, thin fluid. The cut surface was even 
and diffusely colored red. The consistency was firm and 
friable, the structure indistinct and no milk points were 
present. Red fluid was expressed. Here and there dark 
red-colored, sharply defined parts were observed (blood 
infiltration). Numerous veins were occluded by firm 
thrombi. Red-stained fibrin cylinders and a thin fluid were 
observed in the milk canals and in the cisterns. The loose 
subcutaneous tissue over the udder was swollen, red stained 
and of gelatinous consistency. Red fluid was expressed 
from it. No lesions were found in other parts of the udder. 

In the liquid of the incision a great number of Gram 
positive, uniformly round cocci, arranged in twos or in 
small bunches, were observed (staphylococci). The diag- 
nosis was corroborated by cultures. 

2. Staphylomycosis in the left half of the udder. Diffuse 
udder necrosis with gangrene. 

The cow had to be slaughtered. 

The left half of the udder was greatly swollen and of 
firm consistency. The left anterior teat was red and greatly 
swollen. The corresponding lymph-gland was slightly 
swollen. 



POST-MORTEM REPORT 151 

Both left quarters manifested the same lesions, although 
the lesions in the anterior quarter were more advanced than 
those in the posterior quarter. The incision was succulent 
and the juice consisted of a thin red fluid. The cut surface 
was even, uniformly red stained, and of firm but friable 
consistency. The structure was indistinct. No milk 
points were present. Red j nice was expressed. Here and 
there poorly defined grayish-green areas the size of a nut 
were observed, which had a soft elastic consistency and 
crepitated when incised (emphysema). Small excised 
pieces floated in water. These parts presented a putre- 
factive odor. The milk-ducts and the cisterns contained 
grayish-red firm but friable fibrin cylinders; the subcutis 
over the diseased anterior quarter was swollen, red and of 
a gelatinous consistency. A red fluid was expressed. The 
connective tissue of the teat of this quarter showed the same 
lesion (oedema). No lesions were seen in the other parts 
of the udder. 

The fibrin contained a great number of Gram positive 
cocci arranged in irregular bunches (staphylococci). The 
diagnosis was corroborated by culture. 

In the green parts large Gram positive spore-bearing 
baciUi were seen (putrefactive bacilli). 

C. COLIBACILLOSIS 

1. Colibacillosis in the right posterior quarter . 

Only the right posterior quarter was slightly swollen, 
and its consistency somewhat firm. 

The incision at this point was succulent and the juice 
consisted of yellow flocculent milk. In the lower part of 
the cut surface was even, yellowish-gray and somewhat firm. 
The lobuli showed no milk points and yellow fibrin cylinders 
were expressed. In the posterior part a somewhat sharply 
circumscribed area was present which was red stained, of 



162 MASTITIS OF THE COW 

firm but friable consistency and about the size of an egg. 

The lobuli showed the same alterations here as those in 
the yellowish-gray part. Yellowish fibrin was found in 
the milk canals and cisterns. Other parts of the udder 
presented no lesions. 

A comparatively great number of clumpy Gram nega- 
tive bacilli showing rounded ends were found in the fibrin 
and in scrapings taken from the red parts (colon bacilli). 
The diagnosis was corroborated by cultures. 

D. PYOBACILLOSIS 

1. Pyohacillosis in both posterior quarters. 

Both posterior quarters of the udder were moderately 
swollen. Their consistency was firm. The lymph-glands 
were slightly enlarged. 

Both quarters showed the same lesions. The incision 
was covered by thick yellowish-green pus. The lower part 
of the cut surface was even, grayish-white and firm. The 
lobuli showed no milk points, but small yellow pus foci. 
Yellow cylinders of pus were expressed. Yellowish-green 
pus foci ranging in size from a hemp seed to a bean were 
observed here and there. They presented a faint, disagree- 
able odor (not putrefaction) and were surrounded by a 
white, firm, tough connective-tissue capsule. A few milk- 
ducts were thickened and formed large irregular cords 
which, on cross section, presented a yellowish-green centre 
of pus surrounded by a firm, white connective-tissue cap- 
sule, and outside of that by thickened lobuli. Yellow, 
spongy fibrin was found in the teats and milk-ducts. Other 
parts of the udder presented no lesions. 

A great number of small, thin Gram positive bacilli 
were found in the yellowish-green pus (pyogenes bacilli). 

2. Pyohacillosis in the right half of the udder as well as 
in the left posterior quarter. Complication with gangrene. 



POST-MORTEM REPORT 153 

The right anterior quarter of the udder was moderately 
swollen and hard. Both posterior quarters were slightly 
swollen and firm in their inferior parts. 

Right anterior quarter: The incision was smeared by 
a yellowish-green, thick pus. The cut surface was even, 
grayish- white, and firm. The lobuli showed no milk points, 
but yellow pus points instead. Here and there a number 
of yellowish-green pus foci the size of a hemp seed were 
present which were surrounded by a thick, white fibrous 
capsule, the inside of which showed a green pigmentation. 
These foci gave off a disagreeable putrefactive odor. A 
few of these pus foci were cylindrical, extended and formed 
fistulas. Gray spongy fibrin was present in the milk-ducts 
and cisterns. 

Both posterior quarters presented similar but somewhat 
less widely distributed lesions. Other parts of the udder 
showed no alterations. 

In the fibrin and yellowish-green pus a large number 
of small, thin Gram positive bacilli (pyogenes bacilli), as 
well as other bacteria, were observed ( cocci, Gram negative 
rods, putrefactive bacteria). 

E. TUBERCULOSIS 

1. Tuberculosis of the left anterior quarter. Early 
tuberculosis. 

The left anterior quarter of the udder was greatly 
swollen and hard. 

The corresponding lymph-gland was greatly swollen. 
The incision was juicy with lymph. The cut surface was 
gray and showed no caseous foci. Its consistency was soft 
and friable. 

The incision in the diseased quarter of the udder was 
succulent with milk. The lower part of the cut surface 
was even, firm, and gray in color. The lowest part of this 



154 MASTITIS OF THE COW 

area was uniform, and the superior part of it was irregular, 
nodular or coarsely granular. The lobuli in this region 
showed no milk points, but here and there, especially in the 
lower part, a number of small, yellow caseous points or fine 
caseous streaks (caseous necrosis in the collecting tubules) 
were present. Yellow creamy fluid was expressed (soft- 
ened necrosis ) . The superior and greatest part of the cut 
surface was strongly convex, whitish-gray and of very soft 
and elastic consistency. The lobuli of this area were en- 
larged, strongly convex and showed distinct white milk 
points. Milk-ducts and cisterns contained milk. Other 
parts of the udder showed no lesions. 

A number of fine acid-fast rods were found in the yellow 
cream-like fluid (tubercle bacilli). 

2. Tuberculosis in the right posterior quarter. Ad- 
vanced tuberculosis with calcification. 

The right posterior quarter of the udder was greatly 
swollen and hard. 

The corresponding lymph-gland was greatly enlarged. 
Its incision was juicy with lymph and the cut surface showed 
a number of yellow caseous points and yellow branched 
caseous streaks in the cortex which often showed whitish- 
yellow calcareous centres. 

The incision in the diseased quarter was dry and gritty. 
Cut surface even and firm. Its superior portion was irregu- 
lar and nodular. The lobuli of this area showed no milk 
points, but small yellow caseous points or caseous streaks. 
Caseous cylinders were expressed. The inferior part of 
this area was uniform, grayish-yellow and dry. The lobuli 
of this area presented no milk points, but numerous thickly 
placed yellow caseous points and caseous streaks. Other 
lobuli were entirely yellow and showed yellowish-white cal- 
careous centres or calcareous streaks. At numerous points 
yellow, firm caseous foci showing yellowish-white cal- 
careous streaks were found which were surrounded by a 



POST-MORTEM REPORT 155 

thin white connective-tissue capsule. Otherwise the udder 
showed no lesions. 

The cheesy foci showed fine acid- fast rods (tubercle 
bacilli ) . 

3. Tuberculosis of the left posterior quarter with ulcera- 
tion through the skin and complication with gangrene. Ad- 
vanced tuberculosis with softening of the caseous foci. 

The left posterior quarter was greatly swollen and hard. 
Posterior to and on either side of the teat there were two 
fistulous openings about the size of a pencil containing a 
yellow, stinking fluid. 

The corresponding lymph-gland was greatly swollen. 
It was gritty and dry on section (calcium) . For the most 
part the cut surface was yellow, firm and hard, due to 
necrosis and calcification. 

The diseased quarter of the udder was gritty, on section, 
and was smeared by a yellow caseous mass. The lower part 
of the cut surface was even, yellowish-gray and uniform. 
The lobuli showed no milk points, but caseous points were 
present. 

In addition to these, round cavities were seen which 
ranged in size from a pea to a walnut, and contained a 
yellow, thick fluid mass of a plaster-of-Paris consistency, 
due to lime. A thin, white wall of connective tissue sur- 
rounded these cavities. Each fistulous opening communi- 
cated with an oval or cylindrical cavity the size of a hen's 
egg. These contained a dark yellow stinking fluid, show- 
ing a consistency of plaster of Paris. The walls of the 
cavity consisted of thick, white, tough connective tissue, 
the internal surface of which was stained dark bluish-green. 
The superior and smallest part of the cut surface was con- 
vex, whitish-gray, soft and elastic. The lobuli here were 
large and showed distinct milk points. Between this pari 
and the severely diseased area a yellowish-gray, iri'egular, 
granular line of demarcation was visible. A few yellow, 



156 MASTITIS OF THE COW 

free, croupous membranes were found in the milk-ducts and 
cisterns. No lesions were found in the other parts of the 
udder. 

Fine acid-fast bacilli were found in the caseous foci 
(tubercle bacilli). 

F. ACTINOMYCOSIS 

1. Actinomycosis of both posterior qiuirters. 

Both posterior quarters of the udder were slightly 
swollen. The consistency was firm. 

The lymph-glands were not enlarged and on section 
showed no lesions. 

Both posterior quarters showed the same lesions. The 
incisions were somewhat dry. The lower part of the cut 
surface was even, gray and irregular. It showed a number 
of thickly placed yellowish-gray, soft, strongly convex foci 
(actinomycomata) , which ranged in size from a hemp seed 
to a pea and showed discrete yellowish-brown points. Other' 
parts of the udder manifested no lesion. 

Under the microscope brown bodies showed a radiating 
structure and a distinct peripheral layer of club-shaped 
structures (actinomyces fungi). 

2. Actinomycosis of the left anterior quarter. Ad- 
vanced actinomycosis. 

The left anterior quarter of the udder was greatly 
swollen and hard. The corresponding lymph-gland was 
moderately swollen and the cut surface showed a number 
of convex soft yellow points the size of a pea, showing small 
discrete yellowish points. 

An incision in the diseased quarter was dry. The in- 
ferior greater part of the cut surface was yellowish-gray, 
somewhat even, and presented a number of round, soft, 
convex relaxed foci the size of a walnut or larger, which 
contained a number of small, discrete, yellowish-white 
points. The milk-ducts and cisterns contained a yellow 
flocculent fluid. Their mucous membranes presented 



POST-MORTEM REPORT 157 

rounded, soft, gray, relaxed, tumorlike growths from the 
size of a pea to that of a hazelnut, which had grown in 
through wounds in the mucous membranes. On section 
these growths manifested small discrete yellowish-white 
points. Otherwise the udder presented no lesions. 

^licroscopic examination of scrapings from the soft foci 
revealed actinomyces colonies showing rather indistinct 
radiation. 

II. Mixed Infections 

A. CHRONIC INFECTIONS, COMPLICATED WITH ACUTE 
INFECTIONS 

1. Pyohadllosis of the left half of the udder, complicated 
with staphylomycosis in the posterior quarter. 

The cow had to be slaughtered. 

The left half of the udder was hard and swollen, the 
posterior quarter greatly so, and the anterior quarter to a 
moderate degree. 

The corresponding lymph-gland was not swollen and 
it showed no lesions on section. 

The incision in the left posterior quarter was succulent 
and the juice consisted of a red turbid fluid. The cut sur- 
face was even and diffusely reddened. The consistency 
was firm but friable, and the structure indistinct. The 
lobuli presented no milk points, but here and there single 
bright red colored points were seen (pus points). Red 
fluid and dark gray cylinders of pus were expressed. In 
other areas a number of round cavities ranging in size from 
a pinhead to a bean were seen which contained reddish- 
gray thin fluid or thicker caseous matter. The cavities were 
surrounded by a thick, white, tough capsule of connective 
tissue showing a smooth internal surface. A few sharply 
circumscribed areas were dark red, due to blood infiltration. 
A few veins were occluded by firm red-stained thrombi. 



158 MASTITIS OF THE COW 

The entire cut surface of the udder presented a stinking 
odor. The milk-ducts and cisterns contained a thin fluid 
and their mucous membranes were red-stained. 

The lower portion of the cut surface of the left anterior 
quarter was reddish-yellow and firm, and the structure dis- 
tinct. The lobuli showed no milk points, but small yellow 
pus points were frequent. Cylinders of pus were expressed. 
Here and there yellowish-green caseous pus foci the size of 
a pea and surrounded by a connective-tissue capsule were 
observed. The cut surface presented no odor. The mucous 
membranes of the milk-ducts were covered by loose, grayish- 
yellow croupous membranes. Other parts of the udder 
showed no lesions. 

The liquid from the incision in the posterior quarter 
presented a great number of small thin Gram positive 
bacilli (pyogenes bacilli) , together with a moderate number 
of Gram positive round cocci arranged singly or in bunches 
(staphylococci), besides other bacteria (putrefactive bac- 
teria). The diagnosis of the staphylococci was corrobo- 
rated by cultures. 

In the caseous pus of the anterior quarter only small 
thin Gram positive pyogenes bacilli were found. 

B. TWO CHRONIC INFECTIONS 

1. Typical chronic streptomycosis in all four qtuirters, 
complicated with tuberculosis in the right posterior quarter. 

The right posterior quarter of the udder was moderately 
swollen and hard. The other quarters were decreased in 
size, yet still thick and firm. 

The right lymph-gland was enlarged. The incision was 
succulent with l5niiph. On cut section the cortex presented 
small yellow caseous points. The consistency was friable. 
Incision in the right posterior quarter presented a small 
quantity of yellow cream-like pus. The cut surface was 



POST-MORTEM REPORT 159 

even and firm. Its lower part was irregular, nodular and 
yellowish-gray. Deeply the granules were numerous, but 
superficially few. The lobuli here showed no milk points, 
but small yellow caseous points and caseous streaks. The 
superior part of the cut surface was whitish-gray and firm 
as tendon. The lobuli showed no milk points in this area. 
Yellow cream-like pus was expressed. 

The other quarters were also purulent when incised. 
The cut surface was whitisK-gray, even, uniform and fibrous 
in consistency. The lobuli were small and showed no milk 
points. Yellow cream-like pus was expressed. 

Small acid-fast bacilli (tubercle bacilli) were found in 
the caseous foci. 

Gram positive cocci in long chains (streptococci) were 
found in the yellow cream-like pus. 

2. Pyohacillosis in the left posterior quarter complicated 
with tuberculosis. Ulceration through the skin and 
gangrene. 

The left posterior quarter of the udder was greatly 
swollen and hard. Posterior to the teat a fistulous opening 
the size of a goose quill was found which discharged yellow 
stinking pus. 

The corresponding lymph-gland was greatly swollen 
and the incision juicy with lymph. The cut surface pre- 
sented no caseous points. The consistency was friable. 

The incision in the diseased quarter was smeared with a 
yellow, soft caseous mass. The cut surface was even, firm, 
yellowish-gray, and showed a number of round cavities 
ranging in size from a hemp seed to a nut. They contained 
yellowish-green thick pus and were surrounded by a thick, 
white connective-tissue wall (abscesses) . A cavity the size 
of two fists was found in the posterior part, which contained 
yellow, stinking pus, and was surrounded by a fibrous wall, 
the internal surface of which was dark green in color. This 
cavity was in communication with the previously mentioned 



160 MASTITIS OF THE COW 

fistula. Between the abscesses the cut surface was yellow- 
ish-gray and irregularly granular. The lobuli of this area 
showed no milk points, but great numbers of small yellow 
caseous points or caseous streaks instead. Caseous plugs 
were expressed. Gray fibrin was observed in the milk- 
ducts and cisterns. Otherwise the udder presented no 
lesions. 

In the yellowish-green pus from the abscesses numerous 
small, thin Gram positive bacilli were found (pyogenes 
bacilli ) . 

In the yellow, cheesy areas thin acid-fast rods were 
observed (tubercle bacilli). 



CHAPTER XVIII 

A FEW REPORTS OF CONTAGIOUS UDDER-INFECTIONS 
I. Contagious Udder-streptomycosis 

A. REVIEW OF A DESCRIPTION BY M. SANDGREN, 
VETERINARIAN AT YST^\D 

During a period of ca. two months, twenty cows were 
affected with a contagious mastitis. The condition oc- 
curred principally in good milking cows. The disease 
began with intense fever and diminished appetite. It 
spread rapidly from one quarter to another until the entire 
udder was soon affected. The diseased quarters were mod- 
erately swollen. The quantity of milk was lessened and 
it was yellow and mixed with pus and flocculi of fibrin. 

The sample submitted was almost normal in appearance 
and of yellowish-white color. The sediment consisted of a 
moderate amount of yellowish-white pus containing a mod- 
erate number of Gram positive streptococci arranged in 
twos. The diagnosis was corroborated by cultures. 

B. REVIEW OF A DESCRIPTION BY S. LINDKVIST, VETERINARIAN 

AT BROSARP 

An obviously contagious mastitis occurred suddenly in 
a cow stable, and in the course of a few days four cases 
developed. The stalls of the animals affected were situated 
in different parts of the stable. The udders were swollen 
and painful, but not hard. The milk at first was com- 
paratively normal, but became mixed with pus and croupous 
flakes. The animals showed no fever, but a diminution of 
appetite. They showed great weakness. They preferred 
to lie down and could only get up with great difficulty. 

11 161 



162 MASTITIS OF THE COW 

The milk sample was of normal appearance and of a 
grayish-white color. The sediment consisted of a large 
quantity of yellow pus which contained a moderate number 
of Gram positive streptococci arranged as diplococci. 

C. REVIEW OF A DESCRIPTION BY H. WELIN, VETERINARIAN AT 

STORA HOF 

Contagious mastitis was present in a cow stable for three 
years, which affected all the cows. The animals manifested 
a sudden severe swelling and hardness of the udder with 
purulent milk or a slight swelling of the udder with some- 
what normal viscid or flocculent milk. In addition these 
latter cases often showed swollen and painful tarsal joints, 
due to metastatic arthritis. One case died, but was not 
autopsied. In the same stable two similar cases developed. 
The diseased cows showed fever and weakness, swelling of 
the udder, together with swollen, painful joints. The 
animals could scarcely stand, and the quantity of milk was 
decreased. 

The milk sample submitted was nearly normal in ap- 
pearance. The sediment consisted of a moderate quantity 
of whitish-yellow pus, containing many streptococci in short 
chains. 

II. Contagious Udder-pyobacillosis 

REVIEW OF A description BY K. KUHLMAN^ VETERINARIAN 
AT LANGHUNDRA 

In a cow stable containing approximately sixty cows, 
six developed contagious mastitis, by degrees, in one month. 
Usually only one quarter was affected, sometimes two. The 
diseased quarter was swollen and hard, but not painful. 
The milk suddenly became flocculent, then purulent, thick 
and stinking. 

The affected cows were isolated and treated with boric 



CONTAGIOUS UDDER-INFECTIONS 163 

acid injections and iodine embrocations. One cow was 
slaughtered. The enzootic disappeared following this 
treatment. In the same stall similar sporadic cases 
developed. 

The milk sample submitted showed a somewhat normal 
appearance, but was flocculent. The sediment consisted of 
a moderate quantity of pus containing numerous small, thin 
Gram positive bacilli (pyogenes bacilli). The diagnosis 
was corroborated by autopsy of the udder sent in for ex- 
amination following slaughter of the animal. 



LITERATURE 

USED BY AUTHOR IN DRAWING CONCLUSIONS FROM THE 
RESULTS OF HIS EXPERIMENTS 

Andeksson Th. : Enzootisk mastit. Tidskr. f. Vet. med., 1893. 

Bang : Uber die Eutertuberculose der Milchkuh. Zeitschr. f . Thier- 
med. 1885. 

: Aarsagerne til Yverbetaendelse hos Kvaeget. Tidskr. f. 

Vet. 1889. 

Barthel: Om jufrets och mjolkens bakteriologiska forhallanden. 
Sv. Vet. Tidskr. 1906. 

Besson : Technique microbiologique. 1904. 

BiGOTEAU : Om Behandling av Yverbetaendelse. Referat. Maa- 
nedsskr. f. Dyrl. 1906. 

Bongert: Bakteriologische Diagnostik. 1904f. 

Brante: Resectio mammae vaccae. Sv. Vet. Tidskr. 1898. 

Christensen : Smitsom Yverbetaendelse hos Kvaeget. Maaneds- 
skr. f. Dyri. 1895. 

Frank: Handbuch der Tierarztlichen Geburtshilfe. 1901. 

Glage : Uber die Bacillus pyogenes suis Grips, den Bacillus pyo- 
genes Kunneman and den bakteriologischen Befund bei den 
chronischen abzedierenden Euterentzundungen der Milchkuhe. 
Xeitschr. fur. Fleisch- und Milchhygiene. 1903. 

Harms : Lehrbuch der tierarztlichen Geburtshilfe. 1896. 

HoLTH : Bacillus pyogenes og de av den fremdkaldte Vaevsfor- 
andringer. Maanedsskr. f. Dyrlaeger. 1908. 

HoLST : Om Kaedekker og Yverbetaendelse hos Koer som Aarsag 
till akut Mave-Tarmkatar hos Mennesker. Referat. Maa- 
nedsskr. f. Dyrlaeger. 1895. 

Jbel,: Die mikroskopischanatomischen Veranderungen bei gelben 
Gait. 1903. 

Jenssen : Mastitis bei Tieren. Ergebnisse der allgem. Pathologie. 
1899. Maelk og Maelkekontrol. 1903. 

Jenssen og Tobiessen : Om paratyfus. Ugeskr. f . Laeger. 1904. 

Kitt: Bakterienkunde. 1903. Pathologische Anatomic der Haus- 
tiere. 1905-6. 
164 



LITERATURE 165 

Kjerrulf: Handbok i Kottbesiktning. 1891. Milchygienische 

Verbal tnisse in Schweden. 1903. 
Lehmann und Neumann : Bakteriologische Diagnostik. 1907. 
Linde: Die gewebsveranderungen im Euter bei Galactophoritis 

sporadica der Kuh. 1906. 
Lucet: Des mammites aigues. 1891. 
Metchnikoff : Lecons sur la pathologie comparee de I'inflamma- 

tion. 1892. 
Moore : The pathology and differential diagnosis of infectious dis- 
eases of animals. 1906. 
Moussu: Traite des maladies du Betail. 1902. 
NocARD et Lechlainche : Les maladies microbiennes des animaux. 

1903. 
Nystedt: En massforgiftning i Stockholm sfter fortarandet af 

mjolk fran en ko med infektios mastit. Sv. Vet. Tidskr. 1902. 
Ostertag: Handbuch der Fleischbeschau. 1902. 
Ostertag, Breidert, Kaestner und Krautstrunk : Untersu- 

chung uber die klinische und bakteriologische Festellung der 

Tuberkulose des Rindes. 1905. 
Rasmussen: Om aktinomykose. Maanedsskr. f. Dyrlaeger. 1889. 
Ribbert: Lehrbuch der allgemeinen Pathologie. 1905. 
Staheli: Zur Biologic des Streptococcus mastitidis contagiosae. 

1904. 
Steiger : Bakterienbefunde bei der Euterentzundung von Kuh und 

Zeige. 1904. 
Stenstrom : Ar ansvallning af gl. supramam. ett pathognostiskt 

symptom vid tuberculosis uberis. Sv. Vet. Tidskr. 1898. 
Straten : Om Behandling af Yverbetaendelse hos ,Koen med Bor- 

syreindsprojtninger. Maanedsskr. f. Dyrl. 1906. 
Streit: Vergleichende Untersuchungen uber Kolibakterien und 

die gewohnlichen Bakterien der Euteruntzungen der Kuhe. 

1901. 
SuNDBERG : Mikraoorganismerna fran lakarens synpunkt. 1897. 
SvENssoN : Tuberculose mammaire. La lutte contra la tuberculosa 

en Suede. 1905. 
ToBiASSEN : Om en ejendommelig From av Yverbetaendelse hos 

Koen. Maanedsskr. f. Dvrl. 1896. 



166 MASTITIS OF THE COW 

Vennerholm : Die Krankheiten der weiblichen Geschletsorgane 

und der Milchdrusen. 1897. 
ViLLUMSEN : En saeregen Form av Yverbetaendelse. Maanedsskr. 

f. Dyrl. 1896. 
ZscHOKKE : Weitere Untersuchungen uber die Streptokokken des 

gelben Galtes. Schweiz. Arch. f. Tierheilk. Bd. XXXIX. 

1897. 

The translator has used: 
Jensen: Milk Hygiene (Pearson), 1907. 
Ernst: Milk Hygiene (Mohler and Eichhorn), 1914. 
Ward : Pure Milk and the Public Health, 1909. 



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